BMP, TGF-β, shv, shortvein, TGF-beta
ligand - tgf-beta homolog - early on dpp establishes embryonic dorsal/ventral axis -- later defines boundaries between appendage compartments - signals through Smad transcription factors
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.42
Gene model reviewed during 5.47
4.5 (unknown)
588 (aa)
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).
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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).
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 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.
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.
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 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.
Comment: in longitudinal veins
JBrowse - Visual display of RNA-Seq signals
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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.
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.
polyclonal
Haploinsufficient locus.
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.
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.
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.
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.
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.
Candidate gene for posterior lobe area quantitative trait locus.
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.
dpp delimits the dorsal extent of the fat body primordium and sets the border between visceral mesoderm and fat body.
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.
Precise spatial control of dpp expression and responsiveness to it are important determinants regulating patterning in the eye imaginal disc.
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.
dpp regulates multiple transcription factors, which function synergistically to specify the amnioserosa.
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 signal has to travel several cell diameters from its source in order to reach all cells that require its signal.
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.
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.
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 is required in the follicle cells for patterning of anterior eggshell structures.
Molecular lesion associated with alleles of dpp identify residues necessary for TGF-Β/BMP cell signaling.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Mutants do not interact with RpII140wimp.
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.
Mutations in dpp cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.
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.
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.
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 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.
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.
Some people may find "decapentaplegic" objectionable as a fly gene name because "-plegic" is strongly associated with human conditions.
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'.