FB2025_05 , released December 11, 2025
Gene: Dmel\dpp
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General Information
Symbol
Dmel\dpp
Species
D. melanogaster
Name
decapentaplegic
Annotation Symbol
CG9885
Feature Type
FlyBase ID
FBgn0000490
Gene Model Status
Stock Availability
Gene Summary
decapentaplegic (dpp) encodes a ligand of the transforming growth factor-β signaling pathway that signals through Smad transcription factors. It acts as a morphogen that contributes to growth regulation, patterning and stem cell fate. [Date last reviewed: 2019-08-01] (FlyBase Gene Snapshot)
Also Known As

BMP, TGF-β, shv, shortvein, TGF-beta

Key Links
Genomic Location
Cytogenetic map
Sequence location
Recombination map
2-6
RefSeq locus
NT_033779 REGION:2428372..2459823
Sequence
Genomic Maps
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
Gene Ontology (GO) Annotations (78 terms)
Molecular Function (10 terms)
Terms Based on Experimental Evidence (8 terms)
CV Term
Evidence
References
inferred from physical interaction with FLYBASE:tkv; FB:FBgn0003716
inferred from direct assay
inferred from direct assay
inferred from direct assay
inferred from genetic interaction with FLYBASE:dally; FB:FBgn0263930
inferred from physical interaction with FLYBASE:dally; FB:FBgn0263930
inferred from physical interaction with UniProtKB:P54631
inferred from physical interaction with FLYBASE:scw; FB:FBgn0005590
inferred from physical interaction with FLYBASE:gbb; FB:FBgn0024234
inferred from physical interaction with UniProtKB:P07713
inferred from direct assay
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000218063
Biological Process (63 terms)
Terms Based on Experimental Evidence (60 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
involved_in dorsal closure
inferred from genetic interaction with FLYBASE:bsk; FB:FBgn0000229
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:sax; FB:FBgn0003317,FLYBASE:tkv; FB:FBgn0003716
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:put; FB:FBgn0003169
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
involved_in head morphogenesis
inferred from mutant phenotype
involved_in heart development
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
acts_upstream_of_positive_effect imaginal disc fusion, thorax closure
inferred from mutant phenotype
inferred from expression pattern
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:shn; FB:FBgn0003396
inferred from mutant phenotype
inferred from expression pattern
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:yki; FB:FBgn0034970
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with UniProtKB:P27091
Terms Based on Predictions or Assertions (3 terms)
CV Term
Evidence
References
Cellular Component (5 terms)
Terms Based on Experimental Evidence (4 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from electronic annotation with InterPro:IPR015615
is_active_in extracellular space
inferred from biological aspect of ancestor with PANTHER:PTN000218063
Gene Group (FlyBase)
Protein Family (UniProt)
Belongs to the TGF-beta family. (P07713)
Summaries
Gene Snapshot
decapentaplegic (dpp) encodes a ligand of the transforming growth factor-β signaling pathway that signals through Smad transcription factors. It acts as a morphogen that contributes to growth regulation, patterning and stem cell fate. [Date last reviewed: 2019-08-01]
Pathway (FlyBase)
BMP SIGNALING PATHWAY CORE COMPONENTS -
The Bone Morphogenetic Protein (BMP) signaling pathway is one of two branches of Transforming Growth Factor-β family signaling in Drosophila. The binding of a BMP family dimer to a heterodimeric serine/threonine kinase receptor complex results in the phosphorylation of Mad, a member of the Smad family. Mad forms a complex with the co-Smad, Med. This complex translocates into the nucleus and regulates the transcription of target genes in concert with other nuclear cofactors. (Adapted from FBrf0236482.)
Gene Group (FlyBase)
BONE MORPHOGENETIC PROTEINS -
Bone Morphogenetic Proteins (BMPs) are a subfamily of the Transforming Growth Factor (TGF)-β family - a group of extracellular ligands for the TGF-β-Receptor family. The binding of a BMP dimer to a heterodimeric serine/threonine kinase receptor complex results in the phosphorylation of Mad, a member of the Smad family. Mad forms a complex with the co-Smad, Med. This complex translocates into the nucleus and regulates the transcription of target genes in concert with other nuclear cofactors. (Adapted from FBrf0236482.)
Protein Function (UniProtKB)
Required during oogenesis for eggshell patterning and dorsal/ventral patterning of the embryo. Acts as a morphogen during embryogenesis to pattern the dorsal/ventral axis, specifying dorsal ectoderm and amnioserosa cell fate within the dorsal half of the embryo; this activity is antagonized by binding to sog and tsg. Induces the formation of visceral mesoderm and the heart in early embryos. Required later in embryogenesis for dorsal closure and patterning of the hindgut. Also functions postembryonically as a long-range morphogen during imaginal disk development; is responsible for the progression of the morphogenetic furrow during eye development. Patterns the wing imaginal disk along its anterior/posterior axis and has a role in positioning pro-veins. Also required to subdivide the wing disk along the proximal/distal axis into body wall (notum) and wing. Ensures the correct architecture of wing epithelial cells. Has multiple roles in the developing tracheal system, controlling directed tracheal cell migration during embryogenesis and later specifying the fate of fusion cells in the tracheal branches. Required for viability of larvae. Essential for the maintenance and division of germline stem cells in the ovary. Signals via the type I receptor tkv, the type II receptor punt, and in some tissues via the type I receptor sax, in a signaling cascade that leads to activation and repression of target genes.
(UniProt, P07713)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
dpp: decapentaplegic (W.M. Gelbart)
dpp is a complex locus affecting numerous developmental events. Mutations fall into three major genetic and phenotypic groupings: called shortvein (shv), Haplo-insufficiency (Hin) and imaginal disk-specific (disk). Each group maps to a different region of the dpp gene. Hin-region mutations have two distinguishing features: they are defective in normal dorsal-ventral patterning of the embryo, and they generally fail to complement mutations of the shv and disk types. shv-region mutations all show recessive defects in longitudinal wing vein formation. disk-region mutations exhibit pattern deletions in the adult epidermal derivatives of the imaginal disks. The phenotypes of most shv/disk heterozygotes suggest partial or full complementation of the shv and disk lesions. Within each of the three major groupings, several phenotypic classes of alleles have been identified. Complementation between certain combinations of dpp alleles is transvection sensitive (Gelbart, 1982, Proc. Nat. Acad. Sci. USA 79: 2636-40). The genetic properties of the several classes of dpp mutations are outlined below. For a given class, the prototypical recessive phenotypes are inferred from examinations of trans heterozygotes for two different alleles of that class. This procedure obviates possible complications due to the frequent association of dpp mutations with gross chromosomal rearrangements. Particular allelic combinations may deviate from the prototypical descriptions. Hin-region emb: Embryonic lethal mutation. Homozygous viable, but recessive lethal in combination with hin-r alleles, and, in the latter background, exhibits the same weakly ventralized phenotype as hin-r homozygotes. Completely complements all shv- and disk-region mutations. The sole emb allele is associated with a small deletion in Hin-region. Hin: Haplo-insufficient mutations. Hin/+ heterozygotes exhibit dominant embryonic lethality with the same weakly ventralized phenotype as hin-r homozygotes. Dominant lethality is rescued by duplication of dppHin+. Homozygotes are defective in gastrulation and die as embryos with completely ventralized cuticle. In general, Hin alleles do not complement any other dpp mutations. However, Hin alleles associated with small deletions or point mutations exhibit transvection effects in heterozygotes with small deletions or insertions in the shv and disk-regions. Hin mutations are considered the null alleles of the dpp gene. Hin alleles are associated with breakpoints, small deletions or point mutations in the Hin-region. Hin-Df: Haplo-insufficient mutations which are behave identically to breakoint Hin mutations, except that Hin-Df lesions are gross deletions removing the entire dpp gene and adjacent vital loci. hin-r: Recessive mutations behaving as milder versions of the Hin lesions. In homozygotes, hin-r mutations exhibit embryonic lethality with weak ventralization effects (identical to emb/hin-r or Hin/+ heterozygotes). All hin-r mutations engender temperature-sensitive mutant phenotypes when heterozygous with shv- and disk-region mutations. Phenotypes elicited in heterozygotes with small deletions, or insertions in the shv and disk regions are transvection sensitive. All hin-r mutations are cytologically normal and show no alterations in their restriction maps. Some have been associated with point mutations in the Hin-region. shv-region shv-lc: Recessive larval-lethal shortvein alleles which complement all disk-region mutations. Exhibit mutant phenotypes in heterozygotes with all shv, Hin, and hin-r mutations. Mutations generally associated with rearrangement breakpoints. shv-lnc: Recessive larval-lethal shortvein alleles which do not complement disk-region mutations. Also exhibit mutant phenotypes in heterozygotes with all shv, Hin, and hin-r mutations. Mutations generally associated with rearrangement breakpoints. shv-p: Recessive shortvein alleles surviving at least to pharate adult. Only two alleles are known; one (s11) is adult viable; exhibits strong venation defects, and variable head capsule defects, including loss of palps, and misarranged vibrissae. Allelic to all shv, Hin, and hin-r mutations. Complement all disk-region mutations. Both alleles are associated with rearrangement breakpoints. shv-w: Recessive viable and fertile shortvein alleles exhibiting only venation defects. Associated with small deletions of the shv-region. Venation phenotype allelic to all shv, Hin, and hin-r mutations. shv-w/Hin, and shv-w/hin-r mutant phenotypes are transvection sensitive. Only two alleles are known; both are associated with small deletions in the shv-region. Tg: A dominant gain-of-function allele in which the tegula on the wing appears duplicated. Tg/+ wings are held out and down. Distinct in phenotype from heldout (d-ho) homozygotes. Tg completely complements all dpp mutations. The dominant effects of Tg can be reverted by superimposing shv, Hin, or hin-r mutations on the Tg chromosome. The one Tg allele is associated with a rearrangement breakpoint in or near the shv-region. disk-region disk-blk: Recessive viable and fertile allele in which the only mutant phenotype is loss of 80-90% of ommatidia in eye; hence this allele was designated blink by Sparrow (unpublished). Exhibits mutant eye phenotypes in heterozygotes with disk-III, disk-V, Hin, and hin-r mutations. Can exhibit transvection effects. The one disk-blk allele is associated with a small deletion within the disk-region. disk-ho: Recessive viable and fertile alleles in which the only mutant phenotypes are heldout wings and loss of the Sc25 on the dorsal base of the wing. Heldout phenotype displayed in heteroyzgotes with all disk-region mutations except d-blk, and with Hin and hin-r mutations. Can exhibit transvection effects. In addition to the one mutant allele listed here, which is associated with a small deletion within the disk-region, several cytologically normal disk-ho alleles have been associated with mobilization of hobo mobile elements residing in the disk-region. disk-II: Recessive viable alleles. Homozygotes exhibit reductions in wing blade, haltere and male genitalia. Elicit mutant phenotypes in heterozygotes with all disk-region mutations except d-blk, and with Hin and hin-r mutations. Mildest class of disk-region alleles associated with rearrangement breakpoints. disk-III: Recessive viable alleles. Homozygotes exhibit multiple pattern abnormalities in epidermis of head, thorax, and terminalia. Structures absent or reduced include labial palps, arista, eye, wing blade, capitellum of haltere, tarsal claws, male terminalia, and female analia. Elicit mutant phenotypes in heterozygotes with all disk-region mutations, and with Hin and hin-r mutations. Intermediate class of disk-region alleles associated with rearrangement breakpoints. disk-V: Recessive early pupal lethal alleles. Homozygous larvae have greatly reduced imaginal disks. Elicit mutant phenotypes in heterozygotes with all disk-region mutations and with Hin and hin-r mutations. Most severe class of disk-region alleles associated with rearrangement breakpoints. t: Recessive larval-lethal alleles. Allelic to all disk, Hin, and hin-r mutations. The only two known alleles of this class behave identically to disk-V lesions, except for the earlier recessive lethal period. Tentatively classified as part of the disk-region. These two mutations are associated with breakpoints which map between the two tRNAtyr genes residing at the Hin-disk-V boundary. Hence the t designation is used to describe these alleles.
Summary (Interactive Fly)

ligand - tgf-beta homolog - early on dpp establishes embryonic dorsal/ventral axis -- later defines boundaries between appendage compartments - signals through Smad transcription factors

Gene Model and Products
Number of Transcripts
4
Number of Unique Polypeptides
1

Please see the JBrowse view of Dmel\dpp for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Structure
Protein 3D structure   (Predicted by AlphaFold)   (AlphaFold entry P07713)

If you don't see a structure in the viewer, refresh your browser.
Model Confidence:
  • Very high (pLDDT > 90)
  • Confident (90 > pLDDT > 70)
  • Low (70 > pLDDT > 50)
  • Very low (pLDDT < 50)

AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.

Experimentally Determined Structures
Crossreferences
Comments on Gene Model

Gene model reviewed during 5.42

Gene model reviewed during 5.47

Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0077771
3723
588
FBtr0077772
3177
588
FBtr0077773
4230
588
FBtr0077775
3216
588
Additional Transcript Data and Comments
Reported size (kB)

4.5 (unknown)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
UniProt
RefSeq ID
GenBank
FBpp0077451
65.9
588
10.41
FBpp0077452
65.9
588
10.41
FBpp0077453
65.9
588
10.41
FBpp0077455
65.9
588
10.41
Polypeptides with Identical Sequences

The group(s) of polypeptides indicated below share identical sequence to each other.

588 aa isoforms: dpp-PA, dpp-PB, dpp-PC, dpp-PE
Additional Polypeptide Data and Comments
Reported size (kDa)
Comments
External Data
Subunit Structure (UniProtKB)

Heterodimers of scw/dpp are the active subunit, dpp/dpp homodimers elicit a basal response and scw/scw homodimers alone are ineffective in specifying a dorsal pattern. Component of a complex composed of dpp, sog and tsg. Interacts with nord and gbb; the interaction interferes with dpp secretion (PubMed:35037619).

(UniProt, P07713)
Linkouts
Sequences Consistent with the Gene Model
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\dpp using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Expression Data
Testis-specificity index

The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).

-0.79

Transcript Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
wing vein | precursor

Comment: reference states 6-9 hr APF

wing vein | precursor

Comment: reference states >=18-20 hr APF

RT-PCR
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

In the stage 10 invaginated hindgut, dpp expression disappears from most of the dorsal domain, except in narrow lateral regions, but persists in the ventral domain.

In addtion to expression anterior to and close to the A/P boundary of third instar wing discs, dpp expression is observed in a proximal region of the posterior compartment. Similar expression is observed in the haltere disc. Expression in both cases begins in the mid-third-instar larval stage. From the fate map, this region gives rise to proximal adult wing structures including the alula and axillary cord.

dpp transcripts are strongly expressed in the spiracular chambers, spiracular branches, and dorsal trunk branches of the tracheal system. Expression is seen in the spiracular chamber form embryonic stage 13 and appears in the spriacular branch and dorsal trunk branches at stage 14. At stage 17, dpp is absent from the spriacular chamber but persists throughout the length of the dorsal trunk branches.

dpp transcript is expressed at lower levels in the haltere disc than in the wing disc.

dpp expression is observed to form a gradient in the dorsal blastoderm. At later stages, dpp expression is observed in the esophageal visceral mesoderm.

dpp is observed to be expressed in somatic cells of the testis.

dpp is observed to be expressed in somatic cells of the germarium.

Transcript is detected in 12 cell widths at the A/P boundary in third instar wing discs. However, expression is excluded from the D/V boundary that will form the wing margin.

dpp is expressed in the dorsal region of the embryo corresponding to the presumptive dorsal ectoderm.

The dpp transcript is expressed along the anterior-posterior boundary of the wing disc.

In wing and leg imaginal discs, sog transcript is expressed in stripes parallel to the dpp stripe along the compartment border. dpp expression along the A/P border disappears in early prepupae. In late prepupae (6-9 hr AP) dpp is expressed in stripes corresponding to vein primordia. dpp expression in vein primordia reappears in 18-20 hr pupae, and expression continues to be restricted to vein primordia in 25-30 hr pupae. Double labeling experiments with sog and dpp transcripts show that sog and dpp are expressed in a strictly complementary pattern in most of the pupal wing, with the exception of the L5 vein, where there is a one-cell-wide gap between sog and dpp expressing cells.

dpp transcripts are expressed along the anterior-posterior boundary in the central region of the wing disc, and approximately along the anterior-posterior boundary in the leg disc. In the eye-antennal disc, expression is detected in the medial regions and along the morphogenetic forrow. Transcripts are detecting in the larval brain in two lateral and two medial spots. Higher levels of staining are detected in the male genital discs than in the female, and the transcripts are also distributed approximately along the anterior-posterior boundary. dpp expression was also detected in late embryonic stages with high levels of transcripts detected in the cephalic and thoracic segments at stage 11 and 13, and in the embryonic brain at stage 13.

dpp transcripts are missing in the visceral mesoderm but not in the ectoderm of putative dpps4 homozygous embryos.

dpp is expressed in two stripes in the visceral mesoderm, the posterior of which coincides with Ubx expression in parasegment 7. dpp transcripts are undetectable in parasegment 7 in Ubx mutant embryos. The domain of dpp expression in the visceral mesoderm is expanded posteriorly in abd-A mutants.

The dpp transcript expression pattern was analyzed in imaginal discs from early third instar larvae through prepupae. Expression is detected in the ventral wing pouch region of the wing disc in early third instar larvae, and in a stripe along the center of the wing disc, as well as low levels along the posterior edge, in late third instar discs. Leg disc expression is first detected as a stripe limited to the medial region of the disc, and then expands into a discontinuous stripe across the entire disc. In the eye-imaginal disc, expression is detected in the periphery of the eye region and laterally in the antennal region. This expression is maintained through late third instar, and additonal expression is detected medially in the antennal region and along the morphogenetic forrow in the eye region. During imaginal disc eversion continued expression of dpp transcripts in detected. In addition to the expression pattern observed during larval devlopment, expression is detected in an anterior stripe in the wing disc, and the dpp transcript expression pattern is resolved into a band along the proximo-distal axis of the appendages.

By the end of germband shortening, dpp RNA is detected at six distinct sites along the gut tube. The sites of expression in the foregut are within the anlage of the pharynx and the esophagus. The midgut sites are within the anlage of the gastric caeca, and the 2nd and 3rd midgut constrictions, the latter being very weak. dpp RNA is also detected in the ectoderm of the hindgut. Embryos with mutations in the shv region of dpp lack midgut expression and have reduced foregut expression, though the early embryo expression pattern is normal. abd-A mutations cause expansion of the domain of dpp expression in the visceral mesoderm to include the entire posterior midgut.

The dpp transcript is expressed in the central region of the wing disc, along the anterior-posterior boundary.

Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

dpp protein was detected in the extracellular lumenal space between the peripodial and columnar epithelium in leg, wing and eye discs of third instar larvae. In addition dpp protein is expressed intracellularly in the known dpp expression domains including an asymetrically distributed anterior/posterior gradient originating at the A/P boundary in wing discs, with a shallower gradient and wider gradient in the anterior compartment. dpp protein was also detected in the morphogenetic furrow of the eye disc.

dpp protein is present in the visceral mesoderm at and anterior to the second midgut constriction from embryonic stage 14. By stage 16, dpp protein surrounds the adjacent endoderm cells.

dpp and Ubx proteins are expressed in overlapping domains in the visceral mesoderm in parasegment 7. The dpp domain extends further anteriorly by half a parasegment. dpp protein is nearly absent in the visceral mesoderm in Ubx6.28 embryos. In a background where Ubx is ectopically expressed all over the embryo, dpp protein is ectopically expressed in the visceral mesoderm from the anterior end of the midgut to PS 7. In embryos lacking abd-A, the Ubx and dpp expression domains extend to the posterior end of the visceral mesoderm. Mutations that remove both Ubx and abd-A cause a novel dpp expression pattern. Embryos that lack genomic copies of Ubx and abd-A but have ectopic Ubx expression from a hs-Ubx construct have ectopic dpp expression throughout the entire visceral mesoderm.

Marker for
 
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
Reporter: M{dpp-LG}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: M{dpp-LHG}
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{419exd}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{-980/dpp-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{BS1.1}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{BS3.0}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{BS3.1}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp0.8}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp45}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp265lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp303lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp419forward}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp674lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp.3KK-GAL4}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dppshv-lacZ.RD2}
Stage
Tissue/Position (including subcellular localization)
Reference
wing vein

Comment: in longitudinal veins

Reporter: P{dppΔDR}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp-GAL4.PS}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp-lacZ.B}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp-lacZ.BE}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp-lacZ.Exel.1}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{dpp-lacZ.Exel.2}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GAL4-dpp.blk1}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GAL4-dpp.H}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{PZ}dpp10638
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{PZ}P1552
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

JBrowse - Visual display of RNA-Seq signals

View Dmel\dpp in JBrowse
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, Transgenic Constructs, and Aberrations
Classical and Insertion Alleles ( 230 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 138 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of dpp
Transgenic constructs containing regulatory region of dpp
Aberrations (Deficiencies and Duplications) ( 58 )
Inferred from experimentation ( 58 )
Gene disrupted in
Gene partially duplicated in
Inferred from location ( 3 )
Variants
Variant Molecular Consequences
Alleles Representing Disease-Implicated Variants
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Sterility
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
actin filament & tracheal tip cell & embryo, with Scer\GAL4btl.PS
adult thorax & adult epidermis
cytoneme & dorsal mesothoracic disc | somatic clone (with dpphr4)
cytoneme & dorsal mesothoracic disc | somatic clone (with dpphr56)
denticle belt & thorax
embryonic/larval fat body & parasegment 4, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 5, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 6, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 6, with Scer\GAL4zen.Kr.PF
embryonic/larval fat body & parasegment 7, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 7, with Scer\GAL4zen.Kr.PF
embryonic/larval fat body & parasegment 8, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 8, with Scer\GAL4zen.Kr.PF
embryonic/larval fat body & parasegment 9, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 10, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 11, with Scer\GAL4twi.PGa
embryonic/larval fat body & parasegment 12, with Scer\GAL4twi.PGa
eye disc & photoreceptor cell, with Scer\GAL4Act5C.PP
eye disc & subretinal glial cell, with Scer\GAL4Act5C.PP
glial cell & eye | ectopic, with Scer\GAL4Act5C.PP
glial cell & eye | ectopic, with Scer\GAL4GMR.PF
macrochaeta & scutum
parasegment 13 & mesoderm | ventral, with Scer\GAL4twi.PGa
scutellum & macrochaeta, with Scer\GAL4dpp.blk1
Orthologs
Human Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Homo sapiens (Human) (33)
10 of 14
Yes
Yes
1  
9 of 14
No
Yes
1  
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
5  
5 of 14
No
No
5 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2  
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
2  
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
2  
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
1  
1 of 14
No
No
Model Organism Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Rattus norvegicus (Norway rat) (34)
10 of 14
Yes
Yes
9 of 14
No
Yes
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
4 of 14
No
No
4 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Mus musculus (laboratory mouse) (33)
10 of 14
Yes
Yes
9 of 14
No
Yes
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
4 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
Xenopus tropicalis (Western clawed frog) (39)
8 of 13
Yes
Yes
5 of 13
No
Yes
5 of 13
No
No
4 of 13
No
No
4 of 13
No
No
4 of 13
No
No
4 of 13
No
No
2 of 13
No
No
2 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
Danio rerio (Zebrafish) (43)
10 of 14
Yes
Yes
10 of 14
Yes
Yes
9 of 14
No
Yes
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
5 of 14
No
No
4 of 14
No
No
4 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Caenorhabditis elegans (Nematode, roundworm) (5)
6 of 14
Yes
No
5 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
Anopheles gambiae (African malaria mosquito) (6)
11 of 12
Yes
Yes
Arabidopsis thaliana (thale-cress) (0)
Saccharomyces cerevisiae (Brewer's yeast) (0)
Schizosaccharomyces pombe (Fission yeast) (0)
Escherichia coli (enterobacterium) (0)
Other Organism Orthologs (via OrthoDB)
Data provided directly from OrthoDB:dpp. Refer to their site for version information.
Paralogs
Paralogs (via DIOPT v9.1)
Drosophila melanogaster (Fruit fly) (6)
8 of 13
6 of 13
4 of 13
4 of 13
3 of 13
3 of 13
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Allele
Disease
Evidence
References
Potential Models Based on Orthology ( 5 )
Modifiers Based on Experimental Evidence ( 3 )
Disease Associations of Human Orthologs (via DIOPT v9.1 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Functional Complementation Data
Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
Interactions
Summary of Physical Interactions
Interaction Browsers

Please see the Physical Interaction reports below for full details
RNA-protein
Physical Interaction
Assay
References
protein-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
Interaction Browsers

Please look at the allele data for full details of the genetic interactions
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
suppressible
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
External Data
Subunit Structure (UniProtKB)
Heterodimers of scw/dpp are the active subunit, dpp/dpp homodimers elicit a basal response and scw/scw homodimers alone are ineffective in specifying a dorsal pattern. Component of a complex composed of dpp, sog and tsg. Interacts with nord and gbb; the interaction interferes with dpp secretion (PubMed:35037619).
(UniProt, P07713 )
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Class of Gene
Genomic Location and Detailed Mapping Data
Chromosome (arm)
2L
Recombination map
2-6
Cytogenetic map
Sequence location
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
22F1-22F3
Limits computationally determined from genome sequence between P{lacW}Rab5k08232 and P{PZ}dpp10638
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
22F1-22F4
(determined by in situ hybridisation)
22F1-22F2
(determined by in situ hybridisation)
22F1-23A
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Left of (cM)
Right of (cM)
Notes
Stocks and Reagents
Stocks (136)
Genomic Clones (33)
cDNA Clones (24)
 

Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequenced
BDGP DGC clones
Other clones
    Drosophila Genomics Resource Center cDNA clones

    For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.

    cDNA Clones, End Sequenced (ESTs)
    BDGP DGC clones
    RNAi and Array Information
    Linkouts
    DRSC - Results frm RNAi screens
    Antibody Information
    Laboratory Generated Antibodies
    Commercially Available Antibodies
     
    Cell Line Information
    Publicly Available Cell Lines
     
      Other Stable Cell Lines
       
        Other Comments

        Haploinsufficient locus.

        The binding of dpp to GAGs/HSPGs plays a role in protection from group B streptococcus infection and in antimicrobial peptide transcription but not in suppression of PGRP-SA and PGRP-SD transcription.

        A second dpp signal from the dorsal ectoderm to the mesoderm during embryogenesis is required to maintain the boundary between pericardial and dorsal muscle cells. The dpp signal maintains this boundary by two mechanisms; the restriction of cell proliferation and the regulation of gene expression critical for cell fate.

        The dpp product negatively regulates dac expression in the embryonic head.

        The Ubx and dpp products collaborate to repress the tkv repressor, sbb, in the haltere disc. The resulting increased amounts of tkv receptor decrease dpp mobility in the haltere.

        The dpp gene product is widely diffusible in the presence of sog protein but tightly localised in its absence.

        Wing and eye disc peripodial cell survival hinges upon dpp signal reception.

        The dpp gene product can be detected in the lumenal cavity between apposed peripodial and columnar cell layers of both wing and eye discs.

        l(2)gl is required downstream of dpp for the specification of dorsal epidermis.

        gbb has both local and long-range functions during wing development that coincide both spatially and functionally with the established functions of dpp. gbb and dpp act locally along the longitudinal and cross veins to affect the process of vein promotion during pupal development, and act long-range from a single focus along the anterior/posterior compartment boundary to affect the processes of disc proliferation and vein specification during larval development. For the local foci, gbb function is confined to regions of the veins that require the highest levels of dpp signaling. For the long-range focus, gbb function does not appear to affect the high point of the dpp gradient, but instead appear to be required for low points.

        dpp promotes DNA replication and growth of the developing large intestine.

        sog and dpp exert opposing maternal functions to modify Tl signaling and pattern the dorsoventral axis of the embryo.

        sog and dpp reduce translocation of dl protein into the nucleus. Maternally produced dpp protein increases the level of cact protein and reduces the magnitude of the nuclear concentration gradient of the dl protein - sog limits this effect.

        The secreted proteins encoded by hh, wg and dpp are expressed in the peripodial membrane yet they control the expression of Dl and Ser in the disc proper.

        wg is required to activate dpp expression during dorsal closure.

        The dpp gradient may regulate notal wg expression through induction of pnr and ush.

        The primary function of pan protein binding to the dpp visceral mesoderm enhancer is repression throughout the visceral mesoderm.

        Decreased dpp signalling in the distal wing cells or increased dpp signalling in the proximal wing cells causes apoptosis in the wing disc.

        The medial-to-lateral dpp gradient along the anterior-posterior axis in the developing wing is complemented by a lateral-to-medial brk gradient, and the opposition of these two gradients may allow cells to detect small differences in dpp concentration and respond by activating different target genes.

        dpp can control gene expression indirectly by downregulating the expression of brk, which represses dpp targets.

        Clathrin-mediated endocytosis participates in dpp action during A/P pattern formation in wing development. Endocytosis is not required for the reception or intracellular processing of dpp, but for the propagation of the dpp signal.

        The size of the dpp expression domain along the A/P boundaries in endocytosis-mutant wing discs is increased, whereas the expression domain of salm is reduced, indicating that the functional range of dpp activity is limited in the endocytosis-mutant wing disc cells.

        dpp prevents activation of the salivary gland genes by Scr in the dorsal region of parasegment 2. dpp sets the dorsal limit on salivary gland cell recruitment through the put and tkv receptors.

        ci protein is necessary but not sufficient for direct activation of the wing-specific dpp "held out" enhancer.

        brk acts as a dpp antagonist in wing patterning. brk function is most important in regions where the dpp gradient has diminishing levels or where a further spreading of the dpp signal has to be prevented.

        Egfr and wg activities in the adult abdomen (promoting tergite and sternite identities) are opposed by dpp signalling which promotes pleural identity. wg and dpp compete directly by exerting opposite effects on cell fate. Within the tergite, the requirements of wg and Egfr function are complementary: wg is required medially, whereas Egfr is most important laterally. dpp signalling at the dorsal midline controls dorso-ventral patterning within the tergite by promoting pigmentation in the medial region.

        wg and dpp participate in mutual transcriptional repression in the adult abdomen.

        Candidate gene for posterior lobe area quantitative trait locus.

        dpp and N specify the fusion cell fate in the dorsal branches of the developing trachea.

        Activation of the dpp pathway induces the expression of tracheal fusion marker genes, including esg and hdc.

        nej functions as a co-activator during dpp signalling. Mad may recruit nej to effect the transcriptional activation of dpp responsive genes during development.

        Signaling by both dpp and gbb contributes to the development of some tissues, while gbb acts alone in the development of others.

        dpp is required to establish G1 arrest in the anterior part of the morphogenetic furrow, via a novel inhibitory mechanism. A dpp-independent mechanism maintains G1 arrest in the posterior part of the furrow. The mechanism by which dpp mediates G1 arrest in the morphogenetic furrow does not require rux. dpp does not mediate G1 arrest in the eye disc by inducing dap expression.

        gbb and dpp interact genetically. Specific aspects of this interaction are synergistic, while others are antagonistic.

        dpp signalling negatively regulates tkv expression. The level of receptor influences the effective range of the dpp gradient. High levels of tkv sensitize cells to low levels of dpp and limit the movement of dpp outside the wing pouch.

        A high level of dpp expression in the leg disc is required to interact with ectopic wg to induce transdetermination. The high levels of dpp, although not sufficient for transdetermination, play a critical role in dorsalising leg cells to promote transdetermination-competent leg cells.

        dpp/tkv signaling is obligatorily required, while scw/sax signaling is necessary but not sufficient for dorsal patterning in the embryo.

        dpp delimits the dorsal extent of the fat body primordium and sets the border between visceral mesoderm and fat body.

        vn plays a permissive role in the induction of the endoderm by dpp and wg, which in turn up-regulate vn expression in the midgut mesoderm in two regions overlapping the dpp sources.

        slmb coordinates wg and dpp expression in the dorsal-ventral and anterior-posterior axes during limb development.

        The dpp gene product is specifically required to maintain female germline stem cells and promote their division. The dpp signal is directly received by germline stem cells. dpp signaling helps define a niche that controls germ stem cell proliferation.

        Mutations in dpp or its receptor sax accelerate germline stem cell loss and retard stem cell division.

        Transcriptional activation of Ubx is subject to competition between dpp-activated Mad and another Smad whose function as a transcriptional repressor depends on high wg signalling.

        Epistasis tests suggest that CrebA acts near the end of both the dpp and spi signalling cascades to translate the corresponding extracellular signals into changes in gene expression.

        The enhancement of leg disc duplication in l(2)gd1 mutants by ft is mediated by dpp.

        Analysis of dpp mutants reveals dpp function is required for furrow initiation along the ventral-posterior margin of the eye disc.

        dpp autoregulation and dpp-mediated inhibition of wg expression are postulated to be required for the coordinated regulation of furrow initiation and progression.

        Regulatory relationships between hh, dpp and wg in the eye are similar to those found in other imaginal discs such as the leg.

        A cAMP response element (CRE) from a Ubx enhancer mediates dpp-responsive transcription in the embryonic midgut.

        hep is required for normal dpp expression in the leading edge during dorsal closure.

        The early function of dpp is to restrict limb formation to the lateral side of the embryo, later graded expression of dpp expressed at the dorsal edge of the limb primordia specifies more proximal cell identities.

        sgg positively regulates dpp expression and negatively regulates wg expression in the imaginal discs, while dsh activity suppresses dpp expression and promotes wg expression in the imaginal discs.

        Jra in the embryo is a downstream target of the bsk signal transduction pathway during dorsal closure formation. The function of the bsk/Jra pathway is to control the localised expression of dpp. Both in the embryo and during photoreceptor cell determination Jra is not regulated by a pathway that involved rl.

        wg and dpp act directly to provide positional information along the proximal-distal (P-D) axis of the leg. The combined activity of both signals is required in a spatially graded manner to define the distinct domains of gene expression along the P-D axis.

        tld protein cleaves sog protein. Cleavage is stimulated by dpp protein.

        dpp specifies the position of most of the sensory organ precursors (SOPs) in the notum and some of them in the wing. Close to the A/P compartment border of the wing, however, SOPs are specified by hh rather than by dpp alone.

        dpp is required for the synchronization of the cell cycle in the developing eye but not for cell fate specification. dpp only mediates a subset of hh functions in the morphogenetic furrow.

        dpp is sufficient to induce initiation of ectopic morphogenetic furrows and formation of duplicated eye discs selectively along the margins of the eye antennal disc. dpp does not appear to be the principal mediator of hh function in the eye.

        Precise spatial control of dpp expression and responsiveness to it are important determinants regulating patterning in the eye imaginal disc.

        The ability of Mmus\Lef1 to stimulate transcription from the Ubx wg response sequence (WRS) requires dpp signalling.

        dpp, by inducing kay, broadly defines an endodermal region which thus becomes predisposed to express lab.

        The bsk pathway is functionally linked to the dpp pathway, the bsk pathway controls dorsal closure at least in part by regulating dpp expression in the leading edge cells. dpp expression is reduced or absent in leading edge cells of embryos lacking bsk function. Transcription factors Jra and aop are required for dorsal closure. Results suggest that the bsk pathway governs dorsal closure at least partially by regulating dpp expression via phosphorylation of Jra and aop.

        Dorsoventral pattern of esg expression in the blastoderm is determined by three independent repressive cues, dpp, sna and twi.

        dpp regulates multiple transcription factors, which function synergistically to specify the amnioserosa.

        The pattern-organizing mechanism governed by dpp involves a negative-feedback circuit in which dpp induces expression of its own antagonist, Dad.

        dpp plays a dual role during tracheal cell migration. dpp controls the region-specific activation of bnl in the dorsal part of the embryo. dpp expression dorsal and ventral to the tracheal placode at the onset of migration instructs groups of tracheal cells with respect to their migration behaviour. Results suggest that other factors in addition to bnl dictate the direction of migration along the dorsoventral axis: some of these factors might be recognised by tracheal cells only upon the reception of the dpp signal.

        The dpp pathway is induced in the tracheal pit by local presentation of dpp from the adjacent dorsal and ventral ectodermal cells. This pathway patterns the dorsal and lateral branches.

        Expression of esg in the neuroectoderm is studied, the expression pattern prefigures that of the ASC genes. Dorsoventral pattern of esg expression in the blastoderm is determined by three independent repressive cues (dpp, sna and twi).

        Ectopic dpp expression can circumvent defects in htl mutants.

        dpp functions to suppress neurogenesis and maintain expression of genes that promoter dorsal cell fates (dorsalisation) in the neuroectoderm. sog protects the neuroectoderm from an invasive positive feedback loop created by dpp diffusion and autoactivation.

        Distinction between dorsal and ventral fates is maintained through mutual repression by dpp and wg.

        Expression of wg and dpp in their normal domains depends on the hh signal.

        Loss of da disrupts the progression of the morphogenetic furrow and this effect is mediated by the loss of both hh and dpp.

        tkv and dpp mutant clones reveal a role for dpp in the early growth of the eye imaginal disc.

        Normal ommatidial development occurs in the complete absence of dpp. Ectopic activation of the dpp pathway does not lead to ectopic neuronal differentiation.

        dpp receptors put and tkv, or the shn transcription factor, are autonomously required for cell proliferation in the entire developing wing.

        The dpp signal has to travel several cell diameters from its source in order to reach all cells that require its signal.

        Dr is regulated by the dorsoventral patterning genes Egfr and dpp in early embryos.

        Increased levels of ci can induce the expression of dpp independent of hh.

        hh directly effects region 2 somatic cells of the germarium via a signalling pathway which includes ptc and ci, but not wg or dpp.

        A dpp-Ecol\lacZ reporter gene, has been studied to determine the segment-parasegment organisation of the genital discs.

        Ectopic expression of dpp can rescue visceral mesoderm formation of htl mutant embryos.

        High levels of ci activate dpp expression and together ci and dpp positively control ara-caup expression.

        Gsc expression is controlled by dpp, oc, slp1/slp2 and tll.

        hh, wg and dpp are required for the establishment of signaling centres that coordinate morphogenesis in the hindgut epithelium.

        Activation of hh, wg and dpp in the developing hindgut and foregut requires fkh.

        Complementary and mutually exclusive activities of dpp and wg organise axial patterning during leg development.

        dpp participates with wg to induce transdetermination.

        Ectopic expression of wg is all discs reveals a dose-dependent effect of wg on patterning and transdetermination that is mediated by modulation of dpp expression.

        Localised expression of dpp instructs cells about their position along the anterior-posterior wing axis in two distinct ways. One mechanism is based on the local concentration of the secreted protein; the other is based on the ability of the cells to retain an instruction received at an earlier time when their progenitors were in close proximity to the signal. Both mechanisms are involved in axis formation.

        Both dpp and wg are required for the nuclear localization of exd protein in the endoderm. Ectopic expression of dpp and wg expands the domain of nuclear exd. The nuclear import of exd product correlates with the transcription of an exd-dependent reporter gene in the endoderm.

        dpp enhancers ignore the nearer Slh and oaf promoters while activating transposon promoters (P{PZ} insertion in oafE-32). This use of only some promoters in the region strongly supports the notion that promoter specificity is the overriding feature establishing the regulatory autonomy of these genes.

        Overexpression of dpp has little effect on dorsal leg patterning, limited effects on wing patterning but substantial dose-dependent effects on anterior-ventral leg patterning. dpp can act both synergistically with and antagonistically to wg in leg disc patterning.

        dpp acts as a gradient morphogen during wing development. Clonal analysis reveals that dpp, secreted by a stripe of wing cells along the anteroposterior compartment boundary, acts directly and at long range on surrounding cells and elicits qualitatively distinct outputs from these cells as a function of their distance from the dpp source. bi and salm are transcriptionally activated at different distances from the dpp secreting cells.

        dpp restricts the domain of wg during limb patterning. By repressing wg expression in the leg, dpp signalling limits the region that responds to high levels of wg and dpp to the site of distal outgrowth.

        ptc and dpp are subject to differential regulation in the posterior eye disc. Elevated en levels repress dpp, ptc and ci expression but do not disrupt eye morphogenesis.

        Loss of dpp signalling leads to ectopic wg gene expression and loss of wg signalling leads to ectopic dpp gene expression. Increased dpp signalling represses wg transcription and increased wg signalling represses dpp transcription.

        dpp is required in the follicle cells for patterning of anterior eggshell structures.

        grk and sax function control dpp expression in the posterior follicular epithelium during oogenesis.

        Molecular lesion associated with alleles of dpp identify residues necessary for TGF-Β/BMP cell signaling.

        Mad is required for dpp signalling during eye development. Mad-mediated dpp signaling is absolutely required for the initiation of the morphogenetic furrow in the eye, but has only a minor role in its subsequent propagation across the eye disc.

        wg transcription is repressed by dpp in the developing eye.

        dpp functions to promote vein formation. dpp promotes vein fates indirectly by activating rho and sog functions by blocking an autoactivating dpp feedback loop.

        sog and dpp are expressed in complementary patterns during pupal wing vein development and function during the same phenocritical period to influence the vein versus intervein cell fate choice.

        The phenotypic consequences of misexpression of sala and salm suggest that an important outcome of dpp activity is the subdivision of the wing disc into territories smaller than lineage compartments, through the regulation of sala and salm.

        sala and salm are expressed in response to dpp in a central territory of the wing imaginal disc, where they are required for the patterning of the wing.

        Mutations in shn affect multiple events that require dpp signalling as well as the transcription of dpp responsive genes. Genetic interactions suggest the shn plays a downstream role in dpp signalling.

        The dl product binds to multiple sites in the dpp second intron, and these sites are required for ventral dpp repression. The sites are adjacent to the DRE (dpp repression element), also required for ventral repression of dpp. A palindromic sequence (PLS) which overlaps a DRE is sufficient to activate dpp expression. A DRE binding activity has been identified by biochemical purification.

        dpp function is not required for duplication in l(2)gd1 leg discs but is required for overgrowth.

        opa is negatively regulated by Ubx and dpp at the location of the first and third midgut constrictions.

        dpp mutants cause lack of visceral mesoderm and heart, ectopic expression of dpp results in ectopic formation of visceral mesoderm.

        dpp is in the inductive signal from dorsal ectoderm cells to activate tin expression in underlying mesodermal cells.

        An inductive signal from dorsal ectodermal cells is required for activation of tin in the underlying mesoderm. dpp serves as a signalling molecule in this process. The spatial expression of dpp in the ectoderm determines which cells of the mesoderm become competent to develop into visceral mesoderm and the heart.

        bi may acting downstream of dpp in pattern formation during appendage development.

        Data presented by FBrf0083197 supports Geoffroy St-Hilaire's theory of dorsal-ventral inversion between vertebrate and arthropod embryos. Two classes of signalling molecule (dpp and sog) represent counteracting systems that control dorsal-ventral patterning and might have been established in a primitive ancestor before the divergence of the arthropods and vertebrates.

        Binding sites for the grh transcription factor contribute to the ventral repression of dpp.

        Pka-C1 and hh have antagonistic effects on a common substrate which regulates transcription of dpp and wg.

        Pka-C1 is essential during limb development to prevent inappropriate dpp and wg expression. A constitutively active form of Pka-C1 can prevent inappropriate dpp and wg expression but does not interfere with their normal induction by hh. The basal activity of Pka-C1 imposes a block on the transcription of dpp and wg and hh exerts its organizing influence by alleviating this block.

        wg and dpp are involved in the organization of the visual ganglia.

        wg expression is necessary for the induction and maintenance of dpp expression in adjacent cells during optic lobe development.

        Expression of dpp is dorsal and expression of vertebrate dpp homologs is ventral.

        Pka-C1 is an integral component of the mechanism that restricts the expression of dpp, ptc and wg in imaginal discs.

        During embryogenesis, tin expression in the dorsalmost mesoderm depends on proximity to dpp-expressing dorsal ectoderm.

        A dpp midgut enhancer has been localized to a 419bp fragment. A 45bp homeotic response element within the 419bp is capable of responding to Ubx and abd-A in a largely tissue specific manner. Binding sites for Ubx, abd-A and exd products have been identified within the 419bp fragment. Comparison of the midgut enhancer from D.melanogaster and D.virilis reveal conserved sequences in addition to those which bind homeotic proteins in vitro.

        Pka-C1 is a key component of a signal transduction pathway that regulates dpp expression in the appendage and eye discs. Pka-C1is a repressor of dpp expression in the anterior compartment of the wing and leg discs and in cells anterior to the morphogenetic furrow in the eye disc.

        Proventriculus development, for which hh, wg and mys are required, is suppressed by dpp. A novel cell signalling centre in the foregut operates through a distinct genetic circuitry in the midgut to direct the formation of a multiply folded organ from a simple epithelial tube.

        dpp is expressed dorsally and its vertebrate homolog BMP-4 is expressed ventrally. Comparison of sequence similarities suggests that dpp is duplicated generating BMP-2 and BMP-4 in vertebrates.

        The dpp signalling process in the developing midgut is mediated by put and tkv.

        The dpp signal leads to activation of Ance and to the determination of different dorsal cell fates.

        Clonal analysis supports the view that dpp is a direct target of repression by en, and that en defines the posterior extent of the dpp stripe in the wing imaginal disc. The en-hh-ptc regulatory loop that is responsible for segmental expression of wg in the embryo is reused in imaginal disks to create a stripe of dpp expression along the A/P compartment boundary.

        dpp promoter is analysed by reverse genetic and biochemical approaches. The 5' flanking region of dpp contains at least two elements that independently direct phase II expression (expressed in broad longitudinal stripes) and at least one element that can direct phase III expression (expressed in narrow longitudinal stripes). The TATA-less dpp core promoter, which directs phase II expression pattern, also resists activation by a ventral-specific enhancer found within the 5' flanking region. The dpp core promoter may directly contribute to the spatial regulation of dpp expression.

        shn function is critical for cells to respond properly to dpp.

        Both ptc and Pka-C1 are required for the correct regulation of morphogenetic furrow progression, apparently acting via repression of dpp.

        Loss of function of either ptc or Pka-C1 in cells anterior to the furrow results in an ectopic furrow characterised by non-autonomous propagation of dpp expression outside the mutant tissue and ectopic photoreceptor differentiation.

        Loss of Pka-C1 function is sufficient to produce an ectopic morphogenetic wave marked by premature ectopic photoreceptor differentiation and non-autonomous propagation of dpp expression.

        Pka-C1 is required for the correct spatial regulation of dpp expression during eye development.

        Ubx protein directly regulates dpp expression. At least one other activity, possibly exd, is required in conjunction with Ubx for PS7-specific activation. Analysis of dpp also indicates the existence of a distinct regulatory mode for visceral mesoderm expression of dpp that involves general activation within the visceral mesoderm coupled to a spatially specific repressing activity.

        cype acts in the dpp transduction signal pathway.

        wg acts to prevent dpp present at the dorsal and ventral margins in the regions that will form head cuticle from initiating a wave of photoreceptor development. Ectopic wg can inhibit the propagation of normal photoreceptor development. wg and dpp interact to define the region in which the morphogenetic furrow can initiate.

        dpp can exert a long-range organizing influence on surrounding wing tissue, specifying anterior or posterior pattern depending on the compartmental provenance, and hence the state of en activity, of the responding cells. dpp secreted by anterior cells along the compartment boundary has the capacity to organize the development of both compartments. dpp may exert its organizing influence by acting as a gradient morphogen in contrast to hh which appears to act principally as a short range inducer of dpp.

        The requirements for tkv in dorsal closure, visceral mesoderm and trachea development assign novel functions to dpp or a closely related member of the TGFβ superfamily.

        dpp is expressed dorsally and controls the differentiation of dorsal structures. The vertebrate homolog, BMP-4, is expressed ventrally and has ventralising activity. This situation is thought to have evolved due to an inversion of the dorsoventral axis. The inversion occurred during early chordate evolution, the chordates turned upside down and henceforth were carrying the nerve cord on their dorsal side.

        scw and dpp act together to establish distinct response boundaries within the dorsal half of the embryo, perhaps by forming heterodimers that have a higher activity than homodimers of either molecule alone.

        Ectopic expression of hh can induce ectopic wg and dpp expression in anterior cells and reorganise the anterior compartment pattern. Loss of endogenous hh blocks wg and dpp expression along the compartment boundary and impedes growth and patterning in both compartments.

        The regulatory autonomy between dpp and oaf (the dpp enhancers have no effect on oaf transcription) is due to promoter specificity and not an intervening chromatin boundary sequence.

        hh is acting as a regulator of dpp expression and dpp acts as an organising molecule controlling growth and patterning in the wing imaginal disc.

        Targeted ectopic expression of dpp in wing imaginal discs using the Scer\GAL4 system causes overgrowth and pattern duplications in both anterior and posterior compartments of the wing disc. Ectopic expression of hh in the anterior compartment of the wing disc causes similar alterations.

        ptc controls dpp expression in the imaginal discs and restricted expression of dpp near the anterior-posterior compartment boundary is essential to maintain the wild type morphology of the wing disc.

        The dpp gene has a visceral mesoderm-specific enhancer that is regulated by Ubx and abd-A in vivo.

        Combined action of wg-expressing cells in the leg ventral anterior compartment and dpp-expressing cells in the leg dorsal-anterior compartment activates expression of Dll.

        The tld protein appears to function by forming a complex containing dpp product, via protein-interacting EGF and C1r/s domains. The protease activity of the tld product is necessary, either directly or indirectly, for the activation of the dpp complex.

        dpp is required for the maintenance of the wing antero-posterior compartment boundary. hh mediates the interaction between anterior dpp-expressing cells and posterior en-expressing cells.

        Expression of dpp in the dorsal or terminal regions of the blastoderm embryos requires an element in the second intron of dpp. Expression in the lateral ectoderm during germ band shortening requires 479bp of sequence upstream of the most proximal dpp promoter (P1).

        wg and dpp are required for target field neurons in the developing brain to adopt their proper fates and to send axons into the developing target structure.

        A 419bp sequence from the dpp promoter is sufficient to direct Ecol\lacZ expression in the embryonic midgut mesoderm.

        Antp, Ubx, abd-A, dpp and wg are required for proper tsh expression.

        Specification of distinct cell fates in response to different concentrations of dpp product may be achieved combinatorially by the sax and tkv receptors.

        dpp is a target gene of the homeotic selector genes and is regulated by exd.

        Expression of abd-A prevents dpp transcription in the whole visceral mesoderm, even when high and uniform levels of Ubx, that activate dpp, are present.

        Ectopic expression of dpp causes the entire midgut to take on the characteristics of the parasegment 7/8 midgut.

        Ectopic expression of dpp eliminates Scr and Antp expression, attenuating abd-A expression, inducing Ubx, dpp, wg and tsh expression in the visceral mesoderm and inducing lab expression in the apposing endoderm. The result is failure of all of the morphogenetic events except formation of midgut constriction 2.

        dpp is involved in induction of dorsal cell fate in the ventral/lateral ectoderm of embryos.

        Ectopic expression of dpp in the ectoderm and mesoderm demonstrates that dpp regulates expression of mesodermal genes.

        Molecular and phenotypic data suggest that sax encodes a receptor for dpp.

        Proper spatial regulation of nub involves the interaction between the mesoderm and the endoderm, but dpp is not the signal that dictates central nub repression across germ layers.

        The presumptive tips of both the leg and wing are characterized by the close association of cells expressing wg, dpp and al. Ectopic expression of wg can induce both ectopic al expression and a duplication of the proximodistal axis, but only in regions with high levels of dpp.

        Thoracic imaginal primordia are allocated in the embryo in response to signals from the wg and dpp gene products.

        dpp and hh drive the progression of morphogenesis in eye development. The primary mediator of furrow movement is dpp.

        Clonal analysis suggests that dpp and hh gene products act as diffusible signals. hh induces the expression of dpp.

        The second intron of dpp contains multiple general enhancer elements as well as multiple dl-dependent ventral repressor elements (VRE).

        Cis-regulatory elements directing expression of dpp in parasegments 4 and 7 of the visceral mesoderm are separable, and regulated by dpp itself, and Ubx and abd-A respectively. dpp both responds to and regulates Ubx in parasegment 7.

        hh acts upstream of gl, sca, h and dpp in the developing eye. dpp is expressed before furrow initiation.

        Two cis-acting upstream regulatory regions have been defined, one required for dpp expression in the visceral mesoderm of the gastric caecae primordia and one required for dpp expression in the visceral mesoderm of parasegment 7. Both act over a distance of up to 10kb on all four of the dpp promoters examined.

        Highly purified recombinant dpp and gbb proteins can induce the formation of cartiledge, bone and bone marrow in mammals, as assayed in the rat subcutaneous bone induction model.

        dpp and wg together partly mediate positive autoregulation of Ubx.

        The upstream sequence of Ubx contains separate response elements for dpp and wg which function independently, though both positive and negative interactions take place between them.

        dpp is an integral part of a gradient that specifies many different cell fates via intercellular signalling. High levels of dpp specify amnioserosa, while progressively lower levels specify dorsal and lateral ectoderm. This potential is highly dosage sensitive. The zygotic dpp gradient and the maternal dorsal gradient specify distinct, non-overlapping domains of the dorsal-ventral pattern.

        dpp alleles display relative phenotypic strengths; this may be correlated to the progressive loss of dorsal pattern elements in the ventralised mutants.

        dpp can both define embryonic polarity and organise patterning within the ectoderm.

        Injection of dpp transcripts into young embryos causes concentration-dependent dorsalisation.

        tld, srw and sog are required to generate a gradient of dpp activity which directly specifies the pattern of the dorsal 40% of the embryo.

        dpp is a complex locus affecting numerous developmental events. Mutations fall into three major genetic and phenotypic groupings: called shortvein (shv), Haplo-insufficiency (Hin) and imaginal disk-specific (disk). Each group maps to a different region of the dpp gene. Hin-region mutations have two distinguishing features: they are defective in normal dorsal-ventral patterning of the embryo and they generally fail to complement mutations of the shv and disk types. shv-region mutations all show recessive defects in longitudinal wing vein formation. disk-region mutations exhibit pattern deletions in the adult epidermal derivatives of the imaginal discs. The phenotypes of most shv/disk heterozygotes suggest partial or full complementation of the shv and disk lesions. Within each of the three major groupings, several phenotypic classes of alleles have been identified. For a given class, the prototypical recessive phenotypes are inferred from examinations of transheterozygotes for two different alleles of that class. This procedure obviates possible complications due to the frequent association of dpp mutations with gross chromosomal rearrangements. Particular allelic combinations may deviate from the prototypical descriptions. Hin-region: emb (Hin-region): Embryonic lethal mutation. Homozygous viable, but recessive lethal in combination with hin-r alleles, and, in the latter background, exhibits the same weakly ventralized phenotype as hin-r homozygotes. Completely complements all shv- and disk-region mutations. The sole emb allele is associated with a small deletion in Hin-region. Hin (Hin-region): Haplo-insufficient mutations. Hin/+ heterozygotes exhibit dominant embryonic lethality with the same weakly ventralized phenotype as hin-r homozygotes. Dominant lethality is rescued by duplication of dppHin+. Homozygotes are defective in gastrulation and die as embryos with completely ventralized cuticle. In general, Hin alleles do not complement any other dpp mutations. However, Hin alleles associated with small deletions or point mutations exhibit transvection effects in heterozygotes with small deletions or insertions in the shv and disk-regions. Hin mutations are considered the null alleles of the dpp gene. Hin alleles are associated with breakpoints, small deletions or point mutations in the Hin-region. Hin-Df (Hin-region): Haplo-insufficient mutations which behave identically to breakpoint Hin mutations, except that Hin-Df lesions are gross deletions removing the entire dpp gene and adjacent vital loci. hin-r (Hin-region): Recessive mutations behaving as milder versions of the Hin lesions. In homozygotes, hin-r mutations exhibit embryonic lethality with weak ventralization effects (identical to emb/hin-r or Hin/+ heterozygotes). All hin-r mutations engender temperature-sensitive mutant phenotypes when heterozygous with shv- and disk-region mutations. Phenotypes elicited in heterozygotes with small deletions, or insertions in the shv and disk regions are transvection sensitive. All hin-r mutations are cytologically normal and show no alterations in their restriction maps. Some have been associated with point mutations in the Hin-region. shv-region: shv-lc (shv-region): Recessive larval-lethal shortvein alleles which complement all disk-region Exhibit mutant phenotypes in heterozygotes with all shv, Hin and hin-r mutations. shv-lnc (shv-region): Recessive larval-lethal shortvein alleles which do not complement disk-region mutations. Also exhibit mutant phenotypes in heterozygotes with all shv, Hin and hin-r mutations. Mutations generally associated with rearrangement breakpoints. shv-p (shv-region): Recessive shortvein alleles surviving at least to pharate adult. one (s11) is adult viable; exhibits strong venation defects and variable head capsule defects, including loss of palps and misarranged vibrissae. Allelic to all shv, Hin and hin-r mutations. Complement all disk-region mutations. Both alleles are associated with rearrangement breakpoints. shv-w (shv-region): Recessive viable and fertile shortvein alleles exhibiting only venation defects. Associated with small deletions of the shv-region. Venation phenotype allelic to all shv, Hin and hin-r mutations. shv-w/Hin and shv-w/hin-r mutant phenotypes are transvection sensitive. Only two alleles are known; both are associated with small deletions in the shv-region. Tg (shv-region): A dominant gain-of-function allele in which the tegula on the wing appears duplicated. Tg/+ wings are held out and down. Distinct in phenotype from heldout (d-ho) homozygotes. Tg completely complements all dpp mutations. The dominant effects of Tg can be reverted by superimposing shv, Hin, or hin-r mutations on the Tg chromosome. The one Tg allele is associated with a rearrangement breakpoint in or near the shv-region. disk-region: disk-blk (disk region): Recessive viable and fertile allele in which the only mutant phenotype is loss of 80-90% of ommatidia in eye; hence this allele was designated blink by Sparrow (unpublished). Exhibits mutant eye phenotypes in heterozygotes with disk-III, disk-V, Hin, and hin-r mutations. The one disk-blk allele is associated with

        The zygotically acting DV genes repress ac expression within specific DV domains.

        The promoter of the lab gene contains a cis-acting site that is required for regulation by dpp.

        The effect of the terminal system on the expression of sna and dpp, is mediated by a reduction in dl activity by the terminal system.

        Mutants do not interact with RpII140wimp.

        appropriate en activity is required for proper restriction of the dpp expression domain as well as being required for maintenance of the posterior compartment fate.

        The relationship of the dpp expression domain in imaginal disks to the process of anterior posterior compartmentization has been determined.

        dpp is a primary patterning gene for dorsal ectoderm; expression is unaffected by mutations in zygotic dorsal-ventral genes.

        Polar expression of dpp requires genes of the terminal group. dpp is required for the normal ontogeny of the zen pattern and fating of the amnioserosa.

        Mutations in dpp cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.

        The Ubx, abd-A, dpp, wg and lab gene products are involved in the induction process between the visceral mesoderm and the gut epithelium in the embryo.

        dpp expression is dependent on Ubx in parasegment 7, homozygous Ubx- embryos have no detectable dpp transcription in parasegment 7.

        The complete dpp expression pattern is generated by an array of 3' regulatory elements that differ in their potency in specific disks and in certain positions within disks.

        Mutations that eliminate visceral mesoderm expression of dpp lead to defects in midgut morphogenesis and alter spatially localised expression of Scr, Ubx and Antp in the visceral mesoderm.

        Mesodermal expression of dpp is required for expression of lab in endodermal cells. Extracellular dpp protein is required for gut morphology by regulating homeotic gene expression in the visceral mesoderm and endoderm of the developing midgut.

        dpp has been expressed in the S2 cell expression system using inducible promoter. Results demonstrate that the dpp protein is both cleaved and secreted.

        Spatially restricted expression of dpp in the visceral mesoderm is regulated by the homeotic genes Ubx and abd-A. Ubx induces dpp expression in the visceral mesoderm cells of the anterior midgut while abd-A represses dpp expression. A consequence of dpp expression is the induction of lab in the underlying endoderm cells. abd-A function is required for expression of wg in the visceral mesoderm posterior to dpp expressing cells.

        dpp is involved in the regulatory hierarchy responsible for the asymmetric distribution and function of zygotic regulatory gene products along the DV axis of early embryos.

        dpp is required for the maintenance and refinement of the zen expression pattern during cellularization and gastrulation.

        Null mutations of dpp are called "dppHin" alleles as they are haplo-insufficient. Hypomorphic mutations map to the Hin region but are recessive so are called "dpphin-r" alleles. Mutations in the disk region are recessive. Mild alleles are defective only in wing posture, these are "dppd-ho" alleles. Mild alleles, lesions in the disk II region, affect the wing, haltere and male genital derivatives. Intermediate alleles, lesions in the disk III region, affect all major appendages, but they do survive to adulthood. Severe alleles, lesions in the disk V region, cause severe defects in all appendages.

        dpp imaginal discs were examined for evidence of cell death in mutants within the dpp 'disk' region: loss of appendages is a result of massive apoptotic cell death in the corresponding regions of the imaginal disc during mid-third larval instar.

        dpp gene has been functionally dissected: 8kb region is able to provide all the dpp product required for correct development and survival to adulthood. One copy of dpp is sufficient to provide a normal ventral pattern of denticle belts, two copies permits larval hatching.

        dpp activity is required early in development for the formation of dorsal epidermal tissue.

        The dpp protein contributes to correct morphogenesis as a secreted factor involved in the differential regulation of cell growth.

        Allelic complementation at dpp is demonstrated to be a transvection effect, structural heterozygosity disrupts complementation.

        Relationship to Other Genes
        Source for database merge of
        Additional comments

        The haplo-insufficient Minute locus proposed to map near dpp (previously called M(2)LS1 or M(2)23AB, FBrf0023910) is now thought to be the haplo-lethal, but not phenotypically Minute, loss of dppHin function.

        dpp can promote ventral fates in Xenopus and injection of sog mRNA counteracts the ventralising effects of dpp.

        Nomenclature History
        Source for database identify of
        Nomenclature comments

        Some people may find "decapentaplegic" objectionable as a fly gene name because "-plegic" is strongly associated with human conditions.

        Etymology

        Adult viable dpp mutants are characterised by multiple epidermal defects in structures derived from 15 of the 19 imaginal discs found in larvae, because of this the mutation has been called decapentaplegic (15 defects). dpp is allelic to 'heldout' mutations but because the name 'heldout' does not connote the myriad effects of the mutation the locus 'heldout' has been renamed 'decapentaplegic'.

        Synonyms and Secondary IDs (35)
        Reported As
        Symbol Synonym
        DPP-C
        Dpp
        (Arnce et al., 2025, Bradic and Rewitz, 2025, Hounsell and Fan, 2025, Park et al., 2025, Slack, 2025, Balakireva et al., 2024, Fu et al., 2024, Jans et al., 2024, Jiang, 2024, Jiménez-Jiménez et al., 2024, Kumar et al., 2024, Schnider et al., 2024, Umargamwala et al., 2024, Avellino et al., 2023, Cabrita and Martinho, 2023, Gude et al., 2023, Guichard et al., 2023, Matsuda and Affolter, 2023, Nandy and Roy, 2023, Sen, 2023, St Johnston, 2023, Yusupova and Fuchs, 2023, Zhai et al., 2023, Chen et al., 2022, Daly et al., 2022, Enomoto and Igaki, 2022, Kharrat et al., 2022, Kimble and Nüsslein-Volhard, 2022, Koranteng et al., 2022, Ma et al., 2022, Montanari et al., 2022, Romanova-Michaelides et al., 2022, Yasugi and Sato, 2022, Zhang and Edgar, 2022, Boumard and Bardin, 2021, Connacher and Goldstrohm, 2021, Costa-Rodrigues et al., 2021, Cox et al., 2021, Fan et al., 2021, Finger et al., 2021, Gan et al., 2021, Gautam et al., 2021, Gong et al., 2021, Herrera and Bach, 2021, Hoshino and Niwa, 2021, Johnson, 2021, Kaltschmidt et al., 2021, Kochendoerfer et al., 2021, Kramer et al., 2021, Léopold, 2021, Loganathan et al., 2021, Madamanchi et al., 2021, Malin and Desplan, 2021, Mase et al., 2021, Mishra et al., 2021, Muñoz-Nava et al., 2021, Rossi et al., 2021, Row et al., 2021, Sahu et al., 2021, Sharma et al., 2021, Song and Hyeon, 2021, Souidi and Jagla, 2021, Surkova et al., 2021, Vidaurre and Chen, 2021, Zhang et al., 2021, Antel and Inaba, 2020, Bajpai and Sinha, 2020, Cang and Nie, 2020, Chen and Desplan, 2020, Coelho, 2020, Colombani and Andersen, 2020, Cui et al., 2020, Dalui et al., 2020, Fancher and Mugler, 2020, Gohel et al., 2020, Gou et al., 2020, Gutiérrez-Martínez et al., 2020, Horne-Badovinac, 2020, Jasper, 2020, Lan et al., 2020, Luo et al., 2020, Malita and Rewitz, 2020, Merkle et al., 2020, Morata and Calleja, 2020, Nandy and Roy, 2020, Pan et al., 2020, Parker and Struhl, 2020, Pastor-Pareja, 2020, Stathopoulos and Newcomb, 2020, Sun et al., 2020, Xu et al., 2020, Yan et al., 2020, Zhou et al., 2020, Nakato et al., 2019, Nil et al., 2019, Pinal et al., 2019, Sato et al., 2019, Wang et al., 2019, Abed et al., 2018, Ahmed-de-Prado and Baonza, 2018, Diwanji and Bergmann, 2018, Fan et al., 2018, Powers and Srivastava, 2018, Rojas-Ríos and Simonelig, 2018, Ruiz-Losada et al., 2018, Sekiguchi and Yamada, 2018, Stuelten et al., 2018, Ahmad, 2017, Amourda and Saunders, 2017, Follansbee et al., 2017, Gervais and Bardin, 2017, Gilmour et al., 2017, Houtz et al., 2017, Li et al., 2017, Liu and Jin, 2017, Liu and Jin, 2017, Monsivais et al., 2017, Siddall and Hime, 2017, Suzuki and Sato, 2017, Takemura and Nakato, 2017, Upadhyay et al., 2017, Zaytseva and Quinn, 2017, Bonfini et al., 2016, Casas-Tintó et al., 2016, Chen et al., 2016, Clavería and Torres, 2016, Dabrowska et al., 2016, Di Gregorio et al., 2016, Fried et al., 2016, Han et al., 2016, Jiang et al., 2016, Kawamoto et al., 2016, Lacy and Hutson, 2016, Li and Jasper, 2016, Mbodj et al., 2016, Sharifkhodaei et al., 2016, Tauscher et al., 2016, Yadav et al., 2016, Yu et al., 2016, Amoyel and Bach, 2015, Apitz and Salecker, 2015, Boija and Mannervik, 2015, Dorn and Dorn, 2015, Enomoto et al., 2015, Gilboa, 2015, Greenspan et al., 2015, Hariharan, 2015, Irvine and Harvey, 2015, Jasper, 2015, Lee et al., 2015, Lo et al., 2015, Matsuda et al., 2015, Meinhardt, 2015, Singh, 2015, Su, 2015, Tokusumi et al., 2015, Van De Bor et al., 2015, Zhou et al., 2015, Boekhoff-Falk and Eberl, 2014, Herranz et al., 2014, Kornberg and Roy, 2014, Kux and Pitsouli, 2014, Pargett et al., 2014, Pichaud, 2014, Roy et al., 2014, Tamori and Deng, 2014, Ting et al., 2014, Bausek, 2013, Bilioni et al., 2013, Denholm, 2013, Doumpas et al., 2013, Fossett, 2013, Hombría and Sotillos, 2013, Ibrahim et al., 2013, Lawrence and Casal, 2013, Levayer and Moreno, 2013, Li et al., 2013, Marinho et al., 2013, Mbodj et al., 2013, Morin-Poulard et al., 2013, Muha and Müller, 2013, Palm et al., 2013, Pastor-Pareja and Xu, 2013, Paul et al., 2013, Sato et al., 2013, Shilo et al., 2013, Shim et al., 2013, Solis et al., 2013, Tremmel et al., 2013, Umulis and Othmer, 2013, Zhang et al., 2013, Grewal, 2012, Hironaka and Morishita, 2012, Holmqvist et al., 2012, Kagey et al., 2012, Karim et al., 2012, Kornberg, 2012, Lim et al., 2012, Matunis et al., 2012, Mirth and Shingleton, 2012, Peterson et al., 2012, Raftery and Umulis, 2012, Rojas-Ríos et al., 2012, Sawala et al., 2012, Smith et al., 2012, Worley et al., 2012, Zoller and Schulz, 2012, Baker, 2011, Baker, 2011, Baker and Firth, 2011, Ben-Zvi et al., 2011, Ben-Zvi et al., 2011, Callejo et al., 2011, de Cuevas and Matunis, 2011, Dworkin et al., 2011, Eivers et al., 2011, Eliazer and Buszczak, 2011, Erickson, 2011, Hamaratoglu et al., 2011, Harris and Ashe, 2011, Harterink et al., 2011, Issigonis and Matunis, 2011, Kaneko et al., 2011, Lander et al., 2011, Losick et al., 2011, Morata et al., 2011, Morishita and Iwasa, 2011, Nien et al., 2011, Ogiso et al., 2011, Peluso et al., 2011, Roth, 2011, Roy et al., 2011, Schwank et al., 2011, Takemura and Adachi-Yamada, 2011, Wang et al., 2011, Wang et al., 2011, Wartlick et al., 2011, Wolpert, 2011, Chen and Xu, 2010, Kang and Bier, 2010, Lei and Song, 2010, Ninov et al., 2010, Portela et al., 2010, Quijano et al., 2010, Reim and Frasch, 2010, Sander et al., 2010, Umulis et al., 2010, Zecca and Struhl, 2010, Karpowicz et al., 2009, Lander et al., 2009, Liu et al., 2009, Svendsen et al., 2009, Campbell and Moser, 2008, Casas-Tinto et al., 2008, Cook et al., 2008, Fan and Bergmann, 2008, Harris and Ashe, 2008, Nusinow et al., 2008, Pan and Xie, 2008, Schwank et al., 2008, Serpe et al., 2008, Vielmas et al., 2008, Wang et al., 2008, Warrior et al., 2008, Zahedi et al., 2008, Bulanin and Orenic, 2007, Crickmore and Mann, 2007, de Velasco et al., 2007, Escudero and Freeman, 2007, Estella and Mann, 2007, Estella et al., 2007, Fedic et al., 2007, Fritsch and Ray, 2007, Gerlitz et al., 2007, Gonzales-Gaitan, 2007, Gunaydin et al., 2007, Hafezi and Hariharan, 2007, Halachmi et al., 2007, Kicheva et al., 2007, Kuranaga and Miura, 2007, Lander, 2007, Lan et al., 2007, Lecuit and Le Goff, 2007, Li and Baker, 2007, Liang et al., 2007, Newfeld and Johnson, 2007, Newfeld et al., 2007, Pistillo and Desplan, 2007, Pistillo et al., 2007, Popichenko et al., 2007, Reim et al., 2007, Schlichting and Dahmann, 2007, Shirinian et al., 2007, Smith and Basler, 2007, Tanaka et al., 2007, Wada et al., 2007, Wang et al., 2007, Widmann and Dahmann, 2007, Baehrecke, 2006, Bangi and Wharton, 2006, Bokel et al., 2006, Canty et al., 2006, Curtiss et al., 2006, Davidson and Erwin, 2006, Dobens and Levine, 2006, Giebel and Wodarz, 2006, Joshi et al., 2006, Knoblich, 2006, Lawrence, 2006, Lin et al., 2006, Moses et al., 2006, Niki, 2006, Ogden et al., 2006, Olson, 2006, Seydoux and Braun, 2006, Umulis et al., 2006, Vrailas et al., 2006, Wang and Ferguson, 2006, Zhu et al., 2006, Angelini and Kaufman, 2005, Araujo et al., 2005, de Velasco and Hartenstein, 2005, Eldar and Barkai, 2005, Firth and Baker, 2005, Häcker et al., 2005, Kirkbride, 2005, Mehlen et al., 2005, Strigini, 2005, Thomas, 2005, Trainor, 2004, Voas and Rebay, 2004, Aldaz et al., 2003, Jekely and Rorth, 2003, Levine and Tjian, 2003, Bhandari and Shashidhara, 2001, Saller and Bienz, 2001, Settleman, 2001, Dale, 2000, Robertson and Bier, 2000, Savery and Wharton, 2000, Szuts et al., 1998)
        Hin-d
        M(2)23AB
        Tg
        dpp
        (Brutscher et al., 2025, Dong et al., 2025, George et al., 2025, Klemm et al., 2025, Liu et al., 2025, Rasouliha et al., 2025, Zúniga-García and Riesgo-Escovar, 2025, Alaraby et al., 2024, Collins et al., 2024, Eslahi et al., 2024, Ewen-Campen and Perrimon, 2024, FlyBoard ad hoc nomenclature committee, 2024.7.14, Gomez et al., 2024, Hersperger et al., 2024, Hunt and Mannervik, 2024, Hunt et al., 2024, Jang et al., 2024, Lababede et al., 2024, Malin et al., 2024, Meyer et al., 2024, Popkova et al., 2024, Raicu et al., 2024, Ridwan et al., 2024, Simon et al., 2024, Sui and Dahmann, 2024, Zambrano-Tipan et al., 2024, Adelmann et al., 2023, Attrill, 2023, Bare et al., 2023, Bastin and Eleftherianos, 2023, Bauer et al., 2023, Candia et al., 2023, Lassetter et al., 2023, Manikowski et al., 2023, Messina et al., 2023, Neophytou et al., 2023, Palermo et al., 2023, Petsakou et al., 2023, Qian et al., 2023, Ramezani et al., 2023, Roth, 2023, Velarde and Baonza, 2023, Xue et al., 2023, Yamada et al., 2023, Zhang et al., 2023, Akiyama et al., 2022, Bressan and Araujo, 2022, Catalani et al., 2022, Chen et al., 2022, Colonnetta et al., 2022, Dunipace et al., 2022, Junion and Jagla, 2022, Merino et al., 2022, National Institute of Genetics Fly Stocks, 2022-, Pandey and Jafar-Nejad, 2022, Perlegos et al., 2022, Saha et al., 2022, Senthil Kumar et al., 2022, Toddie-Moore et al., 2022, Varga et al., 2022, Yassin et al., 2022, Bilder et al., 2021, Casares and McGregor, 2021, Casas-Tintó and Ferrús, 2021, Destalminil-Letourneau et al., 2021, Everetts et al., 2021, Fabian et al., 2021, Gavory et al., 2021, Gore et al., 2021, Hertenstein et al., 2021, Irizarry and Stathopoulos, 2021, Matsuda et al., 2021, Mendoza-Garcia et al., 2021, Mukherjee et al., 2021, Pizette et al., 2021, Poliacikova et al., 2021, Ruiz-Losada et al., 2021, Saad and Hipfner, 2021, Scholl et al., 2021, Slaidina et al., 2021, Zecca and Struhl, 2021, Zhang et al., 2021, Zhao et al., 2021, Belles, 2020, Carnesecchi et al., 2020, Chen and Yamashita, 2020, Cohen et al., 2020, Dai et al., 2020, Gheisari et al., 2020, Hayashi et al., 2020, Hinnant et al., 2020, Hoppe et al., 2020, Irizarry et al., 2020, Ishibashi et al., 2020, Khadilkar et al., 2020, Khan et al., 2020, Ladyzhets et al., 2020, La Marca and Richardson, 2020, Li et al., 2020, Li et al., 2020, Lin and Hsu, 2020, Mao et al., 2020, Mehta et al., 2020, Mira and Morante, 2020, Miscopein Saler et al., 2020, Moulton et al., 2020, Ote and Yamamoto, 2020, Ozakman et al., 2020, Port et al., 2020, Robles-Murguia et al., 2020, Rushton et al., 2020, Rust et al., 2020, Schloop et al., 2020, Small and Arnosti, 2020, Statzer and Ewald, 2020, Texada et al., 2020, Tu et al., 2020, Wang and Dahmann, 2020, Zhang and Cai, 2020, Zhang et al., 2020, Zhang et al., 2020, Zhe et al., 2020, Bageritz et al., 2019, Banerjee et al., 2019, Brodskiy et al., 2019, Chang et al., 2019, Chen, 2019, Chen and Zou, 2019, Coelho and Moreno, 2019, Drummond-Barbosa, 2019, Fan et al., 2019, Grandon et al., 2019, Gui et al., 2019, Held and Sessions, 2019, Houtz et al., 2019, Huang et al., 2019, Hu et al., 2019, Jiang et al., 2019, Khan et al., 2019, Leiblich et al., 2019, Li et al., 2019, Li et al., 2019, Mao et al., 2019, Meltzer et al., 2019, Nelson et al., 2019, Romero-Pozuelo et al., 2019, Rotelli et al., 2019, Shcherbata, 2019, Story et al., 2019, Sun et al., 2019, Tegeder et al., 2019, Varga et al., 2019, Whittle and Extavour, 2019, Wu et al., 2019, Yoshinari et al., 2019, Aguilar-Hidalgo et al., 2018, Ameku et al., 2018, Baker et al., 2018, Haines and Eisen, 2018, Jia et al., 2018, Kang et al., 2018, Kaur et al., 2018, Malzer et al., 2018, Mehrotra and Deshpande, 2018, Osman and Pek, 2018, Paul et al., 2018, Pinal et al., 2018, Sander et al., 2018, Sarkar et al., 2018, Setiawan et al., 2018, Takahashi et al., 2018, Tseng et al., 2018, Wang et al., 2018, Waters et al., 2018, Yeung et al., 2018, Zhu et al., 2018, Aggarwal et al., 2017, Al Khatib et al., 2017, Anderson and Wharton, 2017, Auman and Chipman, 2017, Barrio and Milán, 2017, Bosch et al., 2017, Chambers et al., 2017, Dahal et al., 2017, Eder et al., 2017, Kim et al., 2017, Koenecke et al., 2017, Luo et al., 2017, Matsuda and Affolter, 2017, Nie et al., 2017, Osterfield et al., 2017, Pan et al., 2017, Percival-Smith et al., 2017, Requena et al., 2017, Revaitis et al., 2017, Sanial et al., 2017, Smelkinson et al., 2017, Song et al., 2017, Suisse et al., 2017, Tang et al., 2017, Transgenic RNAi Project members, 2017-, van Tienen et al., 2017, Wells et al., 2017, Yang et al., 2017, Zhang et al., 2017, Apitz and Salecker, 2016, Barton et al., 2016, Beira and Paro, 2016, Carrasco-Rando et al., 2016, Djabrayan and Casanova, 2016, Dominguez et al., 2016, Levario et al., 2016, Li et al., 2016, Matsuda et al., 2016, Mottier-Pavie et al., 2016, Moulton and Letsou, 2016, Nakato and Li, 2016, Norman et al., 2016, Quijano et al., 2016, Sandler and Stathopoulos, 2016, Sarov et al., 2016, Shlyueva et al., 2016, Testa and Dworkin, 2016, Tian et al., 2016, Wang et al., 2016, Willsey et al., 2016, Akiyama and Gibson, 2015, Ayyaz et al., 2015, Ayyub et al., 2015, Barr et al., 2015, Bier and De Robertis, 2015, Chatterjee et al., 2015, Denes et al., 2015, Doggett et al., 2015, Dolezal et al., 2015, Foos et al., 2015, Fried and Iber, 2015, Grifoni and Bellosta, 2015, Harmansa et al., 2015, Inaba et al., 2015, Kern et al., 2015, Lee et al., 2015, Liu et al., 2015, Lu et al., 2015, Luo et al., 2015, Matsuda et al., 2015, Mishra et al., 2015, Nagarajan et al., 2015, Pasco et al., 2015, Richard and Hoch, 2015, Ríos-Barrera et al., 2015, Saadaoui et al., 2015, Sawala et al., 2015, Schleede and Blair, 2015, Tsai et al., 2015, Umulis and Othmer, 2015, Verhulst and van de Zande, 2015, Wang et al., 2015, Winstanley et al., 2015, Won et al., 2015, Xia et al., 2015, Zhou et al., 2015, Zimmermann et al., 2015, Ashwal-Fluss et al., 2014, Averbukh et al., 2014, Ballesteros-Arias et al., 2014, Beira et al., 2014, Blaquiere et al., 2014, Cantera et al., 2014, Claudius et al., 2014, Deshpande et al., 2014, Driver and Ohlstein, 2014, Eliazer et al., 2014, Esteves et al., 2014, Fauré et al., 2014, Hamada-Kawaguchi et al., 2014, Haye et al., 2014, Hodar et al., 2014, Ikmi et al., 2014, Jiang et al., 2014, Kim et al., 2014, Künnapuu et al., 2014, Kux and Pitsouli, 2014, Ma et al., 2014, Maier et al., 2014, Mannervik, 2014, Salazar-Jaramillo et al., 2014, Shukla et al., 2014, Tian and Jiang, 2014, Wang et al., 2014, Wisotzkey et al., 2014, Wylie et al., 2014, Aleksic et al., 2013, Bai et al., 2013, Bausek, 2013, Beckwith et al., 2013, Brückner, 2013.7.16, Chauhan et al., 2013, Chen and Jiang, 2013, Curtis et al., 2013, Ducuing et al., 2013, Ettensohn, 2013, Fan et al., 2013, Gafner et al., 2013, Giannios and Tsitilou, 2013, Guo et al., 2013, Herrera et al., 2013, Hevia and de Celis, 2013, Hombría and Sotillos, 2013, Humphreys et al., 2013, Ibrahim et al., 2013, Jin et al., 2013, Li et al., 2013, Li et al., 2013, Marmion et al., 2013, Moran et al., 2013, Müller et al., 2013, Organista and De Celis, 2013, Palm et al., 2013, Pancratov et al., 2013, Paul et al., 2013, Pepperl et al., 2013, Pérez-Garijo et al., 2013, Ramos and Barolo, 2013, Ríos-Barrera and Riesgo-Escovar, 2013, Saunders et al., 2013, Schaub and Frasch, 2013, Shen et al., 2013, Shimmi and Newfeld, 2013, Southall et al., 2013, Spratford and Kumar, 2013, Sung et al., 2013, Suzanne and Steller, 2013, Tsurui-Nishimura et al., 2013, Upadhyai and Campbell, 2013, Webber et al., 2013, Wotton et al., 2013, Xin et al., 2013, Yamamoto-Hino and Goto, 2013, Yu et al., 2013, Zhang et al., 2013, Caldeira et al., 2012, Chen et al., 2012, Christiansen et al., 2012, Cook et al., 2012, Dahal et al., 2012, Hainaut et al., 2012, Hamaguchi et al., 2012, Haskel-Ittah et al., 2012, Hironaka et al., 2012, Holmqvist et al., 2012, Japanese National Institute of Genetics, 2012.5.21, Kristaponyte et al., 2012, Le and Wharton, 2012, Legent et al., 2012, Liang et al., 2012, Li et al., 2012, Li et al., 2012, Maeng et al., 2012, Marchal et al., 2012, Matunis et al., 2012, Murray et al., 2012, Nfonsam et al., 2012, Niepielko et al., 2012, Pennetier et al., 2012, Reeves et al., 2012, Rojas-Ríos et al., 2012, Rushlow and Shvartsman, 2012, Sagner et al., 2012, Salvany et al., 2012, Stinchfield et al., 2012, Stultz et al., 2012, Turki-Judeh and Courey, 2012, Venables et al., 2012, Wang et al., 2012, Wu et al., 2012, Xia et al., 2012, Xia et al., 2012, Zhou et al., 2012, Ahn et al., 2011, Clark et al., 2011, Dejima et al., 2011, Dutko and Mullins, 2011, Eliazer and Buszczak, 2011, Eliazer et al., 2011, Grigorian et al., 2011, Hwang and Rulifson, 2011, Kaczmarczyk and Kopp, 2011, Kirilly et al., 2011, Knox et al., 2011, Layalle et al., 2011, Liu et al., 2011, Luo et al., 2011, Lynch and Roth, 2011, Merabet et al., 2011, Michel et al., 2011, Mrinal et al., 2011, Nien et al., 2011, Ni et al., 2011, Ogiso et al., 2011, Ozdemir et al., 2011, Parker, 2011, Parker et al., 2011, Parrott et al., 2011, Pilgram et al., 2011, Quijano et al., 2011, Roth, 2011, Roy et al., 2011, Roy et al., 2011, Schwank et al., 2011, Semrau et al., 2011, Su et al., 2011, Szuperák et al., 2011, Trivigno and Haerry, 2011, Tsurumi et al., 2011, Vlachos and Harden, 2011, Wang et al., 2011, Wang et al., 2011, Wojcinski et al., 2011, Yang and Su, 2011, Yuva-Aydemir et al., 2011, Zhang et al., 2011, Zhang et al., 2011, Zhang et al., 2011, Zhou and Kalderon, 2011, Ables and Drummond-Barbosa, 2010, Ayers et al., 2010, Baig et al., 2010, Beam and Moberg, 2010, Bergantiños et al., 2010, Biehs et al., 2010, Bunt et al., 2010, Casali, 2010, Chen et al., 2010, Cheng et al., 2010, de Celis and Molnar, 2010, Firth et al., 2010, Haley et al., 2010, Jung et al., 2010, Lennox and Stronach, 2010, Liu et al., 2010, Lopes and Casares, 2010, Mathur et al., 2010, Mathur et al., 2010, Mukai et al., 2010, Mutsuddi et al., 2010, Negreiros et al., 2010, Popov et al., 2010, Raisin et al., 2010, Reed et al., 2010, Rhiner et al., 2010, Rousset et al., 2010, Salzer and Kumar, 2010, Salzer et al., 2010, Sato et al., 2010, Schwank and Basler, 2010, Sen et al., 2010, Seong et al., 2010, Sopory et al., 2010, Terriente-Félix et al., 2010, Usha and Shashidhara, 2010, Vuilleumier et al., 2010, Wagner et al., 2010, Wang and Ward, 2010, Wang et al., 2010, Weiss et al., 2010, Yagi et al., 2010, Yan et al., 2010, Yavari et al., 2010, Zheng et al., 2010, Ayers et al., 2009, Bejarano and Milán, 2009, Bittig et al., 2009, Cruz et al., 2009, Debat et al., 2009, Eivers et al., 2009, Fontenele et al., 2009, Foronda et al., 2009, González et al., 2009, Jaramillo et al., 2009, Jia et al., 2009, Khaliullina et al., 2009, Kolahi et al., 2009, Künnapuu et al., 2009, Liberman et al., 2009, Liu et al., 2009, Maezawa et al., 2009, Mann et al., 2009, Martinez et al., 2009, Mosimann et al., 2009, Nahmad and Stathopoulos, 2009, Ni et al., 2009, Pentek et al., 2009, Pérez-Garijo et al., 2009, Sellin et al., 2009, Smith-Bolton et al., 2009, Song et al., 2009, Svendsen et al., 2009, Twombly et al., 2009, Venken et al., 2009, Yan et al., 2009, Akiyama et al., 2008, Araujo et al., 2008, Bates et al., 2008, Blanco and Gehring, 2008, Bollenbach et al., 2008, Braid and Verheyen, 2008, Brás-Pereira and Casares, 2008, Casas-Tinto et al., 2008, Chau et al., 2008, Chen et al., 2008, Christoforou et al., 2008, Dougherty et al., 2008, Estella and Mann, 2008, Estella et al., 2008, Fan and Bergmann, 2008, Frandsen et al., 2008, Friggi-Grelin et al., 2008, Gallet et al., 2008, González et al., 2008, Haecker et al., 2008, Haley et al., 2008, Hauenschild et al., 2008, Iron et al., 2008, Jiang et al., 2008, Johnson et al., 2008, Kennell et al., 2008, Kim et al., 2008, Kucherenko et al., 2008, Lebreton et al., 2008, Lembong et al., 2008, Liang et al., 2008, Liang et al., 2008, Lim et al., 2008, Liu et al., 2008, López-Onieva et al., 2008, Miles et al., 2008, Minakuchi et al., 2008, Newfeld et al., 2008, Ni et al., 2008, Ogden et al., 2008, Prince et al., 2008, Raj et al., 2008, Sánchez et al., 2008, Sato et al., 2008, Schwank et al., 2008, Sen et al., 2008, Serpe et al., 2008, Shen et al., 2008, Shlevkov and Morata, 2008, Somorjai and Martinez-Arias, 2008, Stultz et al., 2008, Taghli-Lamallem et al., 2008, Takaesu et al., 2008, Tanaka-Matakatsu and Du, 2008, Terriente et al., 2008, Vyas et al., 2008, Wang et al., 2008, Wang et al., 2008, Zeng et al., 2008, Zhao et al., 2008, Aegerter-Wilmsen et al., 2007, Akdemir et al., 2007, Ayala-Camargo et al., 2007, Ballard and Wharton, 2007, Belacortu et al., 2007, Beltran et al., 2007, Bras-Pereira and Casares, 2007, Buceta et al., 2007, Carneiro and Araujo, 2007, Casas-Tinto et al., 2007, Claret et al., 2007, Cordero et al., 2007, Crickmore and Mann, 2007, Drechsler et al., 2007, Engström et al., 2007, Escudero et al., 2007, Estella and Mann, 2007, Eugster et al., 2007, Fernández et al., 2007, Grammont, 2007, Hatini and Nusinow, 2007, Hatton-Ellis et al., 2007, Hayden et al., 2007, Hufnagel et al., 2007, Israeli et al., 2007, Jakobsen et al., 2007, Johnson et al., 2007, Künnapuu et al., 2007, Lee et al., 2007, Lindner et al., 2007, Loncle et al., 2007, López-Onieva et al., 2007, Makhijani et al., 2007, Malpel et al., 2007, Manjon et al., 2007, Merabet et al., 2007, Molnar et al., 2007, Pan et al., 2007, Pfleger et al., 2007, Ramel et al., 2007, Reig et al., 2007, Sandmann et al., 2007, Shravage et al., 2007, Song et al., 2007, Theisen et al., 2007, Tsai et al., 2007, Umemori et al., 2007, Zeitlinger et al., 2007, Zeitlinger et al., 2007, Zeng et al., 2007, Akasaka et al., 2006, Akashi et al., 2006, Anderson et al., 2006, Araujo et al., 2006, Arbouzova and Zeidler, 2006, Bangi and Wharton, 2006, Bernardi et al., 2006, Biemar et al., 2006, Bokel et al., 2006, Bolivar et al., 2006, Bras-Pereira et al., 2006, Callejo et al., 2006, Carneiro et al., 2006, Chen and Schupbach, 2006, Clark et al., 2006, Crickmore and Mann, 2006, Crickmore and Mann, 2006, de Navas et al., 2006, Dudu, 2006, Dussillol-Godar et al., 2006, Dworkin and Gibson, 2006, Dworkin and Gibson., 2006, Ekas et al., 2006, Ference and Barolo, 2006, Friedrich, 2006, Guichard et al., 2006, Jones et al., 2006, Kim et al., 2006, Kirkpatrick et al., 2006, Li and Li, 2006, Mahr and Aberle, 2006, Maurange et al., 2006, Mizutani et al., 2006, Molnar and de Celis, 2006, Molnar et al., 2006, Montell, 2006, Mosimann et al., 2006, Murray et al., 2006, Narbonne-Reveau et al., 2006, Niki, 2006, Niki et al., 2006, Oishi et al., 2006, Panakova and Eaton, 2006, Payne and Braun, 2006, Prothmann et al., 2006, Ramos and Mohler, 2006, Ratnaparkhi et al., 2006, Schimmelpfeng et al., 2006, Scuderi et al., 2006, Singh et al., 2006, Sotillos and de Celis, 2006, Stern, 2006, Stultz et al., 2006, Stultz et al., 2006, Takaesu et al., 2006, Verdier et al., 2006, Vrailas and Moses, 2006, Wahlstrom et al., 2006, Wehn and Campbell, 2006, Wendler et al., 2006, Yao et al., 2006, Yasunaga et al., 2006, Zhang et al., 2006, Zhao et al., 2006, Ayyub et al., 2005, Dawber et al., 2005, Glise et al., 2005, Go, 2005, Gorfinkiel et al., 2005, Horabin, 2005, Jia et al., 2005, Kirilly et al., 2005, Leptin, 2005, Mizutani et al., 2005, Pearson et al., 2005, Qin et al., 2005, Roederer et al., 2005, Rogers et al., 2005, Rogulja and Irvine, 2005, Sano et al., 2005, Scuderi and Letsou, 2005, Sotillos and De Celis, 2005, Stathopoulos and Levine, 2005, Stultz et al., 2005, Takaesu et al., 2005, Thompson et al., 2005, Torroja et al., 2005, Xavier-Neto, 2005, Xie et al., 2005, Yamashita et al., 2005, Zhang et al., 2005, Baines, 2004, Bunt and Hime, 2004, Gurunathan et al., 2004, Hime et al., 2004, Kamimura et al., 2004, Mattila et al., 2004, Motola and Neuman-Silberberg, 2004, Ronshaugen and Levine, 2004, Ryoo et al., 2004, Wang and Struhl, 2004, Yang et al., 2004, Gonzalez-Reyes, 2003, Grienenberger et al., 2003, Vander Zwan et al., 2003, Huet et al., 2002, Jia et al., 2002, Sem et al., 2002, Tuckfield et al., 2002, Gim et al., 2001, Hayashi and Murakami, 2001, Kyoda et al., 2000, Sluss and Davis, 1997, Freeland and Kuhn, 1996, Grimm and Pflugfelder, 1996, Twombly et al., 1996)
        l(2)k17036
        Name Synonyms
        Decapentaplegic
        (Toubarro et al., 2025, Csordás et al., 2021, Morin-Poulard et al., 2021, Zhang and Cai, 2020, Takemura and Nakato, 2017, Zaytseva and Quinn, 2017, Aggarwal et al., 2016, Djabrayan and Casanova, 2016, Fried et al., 2016, Lacy and Hutson, 2016, Nakato and Li, 2016, Matsuda et al., 2015, Roy et al., 2014, Denholm, 2013, Hombría and Sotillos, 2013, Lawrence and Casal, 2013, Levayer and Moreno, 2013, Muha and Müller, 2013, Paul et al., 2013, Lim et al., 2012, Peterson et al., 2012, Rojas-Ríos et al., 2012, Sagner et al., 2012, Smith et al., 2012, Zhou et al., 2012, Zoller and Schulz, 2012, Callejo et al., 2011, Eliazer and Buszczak, 2011, Gehring, 2011, Hamaratoglu et al., 2011, Ogiso et al., 2011, Roy et al., 2011, Schwank et al., 2011, Semrau et al., 2011, Wang et al., 2011, Wolpert, 2011, de Celis and Molnar, 2010, Liu et al., 2010, Ninov et al., 2010, Umulis et al., 2010, Vuilleumier et al., 2010, Weiss et al., 2010, Zecca and Struhl, 2010, Karpowicz et al., 2009, Svendsen et al., 2009, Bickel et al., 2008, Campbell and Moser, 2008, Cook et al., 2008, Estella et al., 2008, Fan and Bergmann, 2008, Frandsen et al., 2008, Harris and Ashe, 2008, Legent et al., 2008, Lim et al., 2008, Lorigan et al., 2008, Miles et al., 2008, Minakuchi et al., 2008, Sato et al., 2008, Schwank et al., 2008, Wang et al., 2008, Wang et al., 2008, Aegerter-Wilmsen et al., 2007, Bernardi et al., 2007, Bulanin and Orenic, 2007, Bunt et al., 2007, de Velasco et al., 2007, Escudero and Freeman, 2007, Fritsch and Ray, 2007, Gerlitz et al., 2007, Hafezi and Hariharan, 2007, Kerszberg and Wolpert, 2007, Künnapuu et al., 2007, Lander, 2007, Lawrence et al., 2007, Lecuit and Le Goff, 2007, Makhijani et al., 2007, Mann et al., 2007, Newfeld and Johnson, 2007, Reig et al., 2007, Baehrecke, 2006, Maurange et al., 2006, Mohit et al., 2006, Montell, 2006, Niki et al., 2006, Olson, 2006, Vrailas et al., 2006, Yasunaga et al., 2006, Kirkbride, 2005, Mehlen et al., 2005, Thomas, 2005, Voas and Rebay, 2004, Levine and Tjian, 2003)
        Decapentaplegic/Bone Morphogenetic Protein
        Haplo-insufficient
        Tegula
        blink
        bone morphogenetic protein
        bone morphogenic protein
        decapentaplegic
        (FlyBoard ad hoc nomenclature committee, 2024.7.14, Colonnetta et al., 2022, Held and Sessions, 2019, Auman and Chipman, 2017, Osterfield et al., 2017, Mottier-Pavie et al., 2016, Wieschaus and Nüsslein-Volhard, 2016, Matsuda et al., 2015, Verhulst and van de Zande, 2015, Hamada-Kawaguchi et al., 2014, Bausek, 2013, Fan et al., 2013, Guo et al., 2013, Humphreys et al., 2013, Ibrahim et al., 2013, Spratford and Kumar, 2013, Suzanne and Steller, 2013, Wotton et al., 2013, Zhang et al., 2013, Li et al., 2012, Maeng et al., 2012, Matunis et al., 2012, Mirth and Shingleton, 2012, Rincon-Limas et al., 2012, Rojas-Ríos et al., 2012, Stultz et al., 2012, Clark et al., 2011, Eliazer et al., 2011, Gehring, 2011, Harterink et al., 2011, Knox et al., 2011, Ni et al., 2011, Tsurumi et al., 2011, Biehs et al., 2010, Jung et al., 2010, Lopes and Casares, 2010, Mathur et al., 2010, Mukai et al., 2010, Mutsuddi et al., 2010, Negreiros et al., 2010, Raisin et al., 2010, Reed et al., 2010, Rousset et al., 2010, Salzer and Kumar, 2010, Salzer et al., 2010, Sen et al., 2010, Seong et al., 2010, Song et al., 2010, Sopory et al., 2010, Wang and Ward, 2010, Yan et al., 2010, Yavari et al., 2010, Fontenele et al., 2009, Foronda et al., 2009, Jia et al., 2009, Khaliullina et al., 2009, Künnapuu et al., 2009, Maezawa et al., 2009, Martinez et al., 2009, Ni et al., 2009, Twombly et al., 2009, Blanco and Gehring, 2008, Gallet et al., 2008, Hauenschild et al., 2008, Ishihara and Shibata, 2008, Johnson et al., 2008, Kim et al., 2008, López-Onieva et al., 2008, Ni et al., 2008, Ogden et al., 2008, Prince et al., 2008, Sánchez et al., 2008, Sen et al., 2008, Shen et al., 2008, Shlevkov and Morata, 2008, Stultz et al., 2008, Taghli-Lamallem et al., 2008, Vyas et al., 2008, Zhao et al., 2008, Ayala-Camargo et al., 2007, Ballard and Wharton, 2007, Bras-Pereira and Casares, 2007, Cao et al., 2007, Fernández et al., 2007, Fuller and Spradling, 2007, Hatini and Nusinow, 2007, Lee et al., 2007, Lindner et al., 2007, Loncle et al., 2007, Anderson et al., 2006, Araujo et al., 2006, Bernardi et al., 2006, Biemar et al., 2006, Bolivar et al., 2006, Canty et al., 2006, Carneiro et al., 2006, Crow et al., 2006, Dworkin and Gibson, 2006, Eissenberg, 2006, Friedrich, 2006, Guichard et al., 2006, Oishi et al., 2006, Payne and Braun, 2006, Prothmann et al., 2006, Ratnaparkhi et al., 2006, Schimmelpfeng et al., 2006, Stultz et al., 2006, Verdier et al., 2006, Vrailas and Moses, 2006, Wendler et al., 2006, Dawber et al., 2005, Horabin, 2005, Qin et al., 2005, Roederer et al., 2005, Sotillos and De Celis, 2005, Stultz et al., 2005, Torroja et al., 2005, Mattila et al., 2004, Motola and Neuman-Silberberg, 2004, Tuckfield et al., 2002, Gim et al., 2001, Grimm and Pflugfelder, 1996)
        heldout
        Secondary FlyBase IDs
        • FBgn0010065
        Datasets (0)
        Study focus (0)
        Experimental Role
        Project
        Project Type
        Title
        Study result (0)
        Result
        Result Type
        Title
        External Crossreferences and Linkouts ( 118 )
        Sequence Crossreferences
        NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
        GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
        RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
        UniProt/GCRP - The gene-centric reference proteome (GCRP) provides a 1:1 mapping between genes and UniProt accessions in which a single 'canonical' isoform represents the product(s) of each protein-coding gene.
        UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
        Other crossreferences
        AlphaFold DB - AlphaFold provides open access to protein structure predictions for the human proteome and other key proteins of interest, to accelerate scientific research.
        DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
        EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
        FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
        FlyMine - An integrated database for Drosophila genomics
        KEGG Genes - Molecular building blocks of life in the genomic space.
        MARRVEL_MODEL - MARRVEL (model organism gene)
        Linkouts
        BioGRID - A database of protein and genetic interactions.
        Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
        DroID - A comprehensive database of gene and protein interactions.
        DRSC - Results frm RNAi screens
        Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
        FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
        FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
        Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
        Flygut - An atlas of the Drosophila adult midgut
        FlyMet - A comprehensive tissue-specific metabolomics resource for Drosophila.
        iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
        Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
        KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
        MIST (genetic) - An integrated Molecular Interaction Database
        MIST (protein-protein) - An integrated Molecular Interaction Database
        SignaLink - A signaling pathway resource with multi-layered regulatory networks.
        References (3,109)