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General Information
Symbol
Dmel\Dl
Species
D. melanogaster
Name
Delta
Annotation Symbol
CG3619
Feature Type
FlyBase ID
FBgn0000463
Gene Model Status
Stock Availability
Gene Snapshot
Delta (Dl) encodes a single pass transmembrane EGF family protein and one of two ligands of the Notch signaling pathway. It regulates cell fate decisions and cell proliferation. Post transcriptional modification (such as by fucosylation, ubiquitination and proteolysis) of the product of Dl is key for its functions. [Date last reviewed: 2019-03-07]
Also Known As
Overflow
Key Links
Genomic Location
Cytogenetic map
Sequence location
3R:19,302,731..19,326,217 [-]
Recombination map
3-66
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Gene Group (FlyBase)
Protein Family (UniProt)
-
Summaries
Pathway (FlyBase)
Notch Signaling Pathway Core Components -
The Notch receptor signaling pathway is activated by the binding of the transmembrane receptor Notch (N) to transmembrane ligands, Dl or Ser, presented on adjacent cells. This results in the proteolytic cleavage of N, releasing the intracellular domain (NICD). NICD translocates into the nucleus, interacting with Su(H) and mam to form a transcription complex, which up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0225731 and FBrf0192604). Core pathway components are required for signaling from the sending cell and response in the receiving cell.
Gene Group (FlyBase)
NOTCH LIGANDS -
Notch (N) receptor ligands are single-pass transmembrane proteins that possess EGF repeats and, with the exception of the atypical Notch ligand, wry, an N-terminal DSL (Delta, Serrate and LAG-2) domain. (Adapted from FBrf0192604 and FBrf0210603).
Protein Function (UniProtKB)
Acts as a ligand for Notch (N) receptor. Essential for proper differentiation of ectoderm. Dl is required for the correct separation of neural and epidermal cell lineages. Fringe (fng) acts in the Golgi to determine the type of O-linked fucose on the EGF modules in N, altering the ability of N to bind with Delta (Dl). O-fut1 also has a role in modulating the interaction.
(UniProt, P10041)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
Dl: Delta
thumb
Dl: Delta
From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 197.
A haplo-insufficient member of the group of neurogenic genes originally described on the basis of its dominant phenotype. Several classes of alleles designated by Vassin and Campos-Ortega based on the phenotype of heterozygous adults: Amorphic and strong hypomorphic alleles display wing veins widened at their junctions with the margin to form delta-like structures; in addition, they show irregular thickening of vein 2, and wings frequently held in divergent attitude; fusion of ommatidia may give rise to disruptions in regular hexagonal array of eye facets; ocelli are slightly enlarged; additional bristles are present on head, thorax, and abdomen; homozygotes die as embryos. Rare antimorphic alleles display the above phenotype in exaggerated form with irregular widening of all longitudinal wing veins, enlarged deltas, regularly divergent wings, smaller rougher eyes, larger and often fused ocelli, and further increase in the numbers of extra bristles; in addition, tarsal joints 2 to 4, but not 5 are fused; homozygotes are embryonic lethals. Rare recessive alleles show low levels of survival as homozygotes or trans heterozygtoes with more severe alleles; survivors usually display a less extreme version of the phenotype exhibited by heterozygotes for amorphic alleles; however, some combinations are wild type in appearance and others (e.g., the antimorphs) are lethal. The embryonic lethality of homozygotes displays the typical neurogenic phenotype with neural hyperplasia accompanied by epidermal aplasia; most or all cells of the neurogenic ectoderm recruited into the neurogenic pathway. Transplantation of homozygous Dl pole cells demonstrate Dl expression during oogenesis (Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32). Dl classed as non-autonomous in that single cells from the neurogenic ectoderm of Dl- embryos are capable of giving rise to both neural and epidermal derivatives when transplanted into the neurogenic region of wild-type embryos, suggesting that Dl- cells are capable of responding normally to information from neighboring cells (Technau and Campos-Ortega, 1987, Proc. Nat. Acad. Sci. USA 84: 4500-04). Transcription in cellular blastoderm seen in the ventrolateral neurogenic ectoderm, with a ventral-to-dorsal gradient of expression, corresponding to the gradient of neurogenic capabilities of the neurogenic ectoderm. During gastrulation a metameric pattern of expression appears, disappears, and reappears; as development proceeds complicated spatial and temporal specificities of expression ensue (Vassin et al., 1987). Interactions with other neurogenic mutations complex; Dl mutations suppress the spl-enhancing effect of E(spl) (Shepard, Boverman, and Muskavitch, 1988, Genetics 122: 429-38) and the expression of Ax (Siren and Portin, 1989, Genet. Res. 54: 23-26); severe alleles fail to survive in heterozygotes with E(spl) loss-of-function alleles [Lehmann, Dietrich, Jimenez, and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 226-29 (fig.)] especially when E(spl) is maternally inherited. Expression of Dl/+ observed to be partially suppressed by duplications for E(spl)+ (Vassin, Vielmetter, and Campos-Ortega, 1985, J. Neurogenet. 2: 291-308), yet, de la Concha, Dietrich, Weigel, and Campos-Ortega (1988, Genetics 118: 499-508) report that extra doses of E(spl)+ enhance the neurogenic phenotype of Dl-. Dl/+ and Dl- phenotypes are suppressed by heterozygous and homozygous deficiencies for H, respectively. For example, H2 is able to suppress the phenotypic effects of Dl9P, either in Dl9P/+ or in Dl9P/Dl9P genotypes; Dl9P/Dl9P is cell lethal in both the eye and the cuticle; Dl9P H2/Dl9P H2 cells, on the other hand, develop nearly normally (Dietrich and Campos-Ortega, 1984). Expression of Dl enhanced by duplications for N+ or H+, and three doses of Dl+ enhance expression of N- and neu-, but reduce the severity of the mam- phenotype. de la Concha, et al. have incorporated many of these observations into a model of neurogenic-gene interaction. Dl alleles interact synergistically with certain Minutes, producing extreme phenotypes and drastically lowered viability (Schultz, 1929, Genetics 14: 366-419); DlOf enhances spaCat (Tsukamoto, 1956, DIS 30: 79).
Dl6B
Like Dl1 except that severity of phenotype in homozygous embryos temperature sensitive. At 18 there is patchy neuralization of cephalic and ventral ectoderm; expression more severe at 25 and extreme at 29. Temperature-sensitive period between pole-cell formation and mesodermal segmentation. Clone of ommatidia homozygous for Dl6B, normal when reared under permissive conditions; in flies raised at 29C, however, ommatidial pattern severely disturbed, producing scarring of the eye surface; ommatidia appear larger than normal and interommatidial bristles missing; homozygous mutant facets contain more than a normal complement of retinula cells-up to 13; cytodifferentiation apparently normal. Cuticular clones exhibit elaboration of extra bristles at bristle-forming sites [Dietrich and Campos-Ortega, 1984, J. Neurogenet. 1: 315-32 (fig.)].
DlB107
The most severe antimorphic allele (Vassin and Campos-Ortega, 1987). All components of the phenotype of heterozygosity for a Dl deletion are present in a drastically increased manner in heterozygotes for DlB107 (or for DlFE30 or DlFE32). All wing veins are irregularly widened, veins 3 and 5 being broadened along their whole lengths (same for vein 2 in DlFE30 and DlFE32) and are occasionally incised posteriorly; the deltas formed at the wing margins are larger and the wings are held spread with complete penetrance. The eyes are smaller and rougher. There is also a severe disturbance of the normal bristle pattern on the head, thorax, and abdomen owing to a further increase in the number of bristles. The ocelli are larger and often fused together, thus forming a half circle. Finally, tarsal segments 2 to 4 are fused, but segment 5 is never found to be affected.
Dlvi: Delta viable
Three alleles survive as homozygotes (Vassin, and Campos-Ortega, 1987). Slight delta-like thickenings at posterior tips of wing veins 2, 3, 4 and 5; roughening of eye. Dlvi homozygotes also show shortening and frequent fusion of tarsal segments. A few homozygous embryos fail to hatch, showing patchy neuralization in cephalic and ventral territories. Dlvi/+ normal. Trans heterozygotes with dominant alleles show extreme wing, eye, and tarsal abnormalities; Dlvi1 lethal in combination with DlF30, DlF32 DlE50-2, and DlB107 (Vassin, and Campos-Ortega, 1987).
Summary (Interactive Fly)
Gene Model and Products
Number of Transcripts
3
Number of Unique Polypeptides
1

Please see the GBrowse view of Dmel\Dl or the JBrowse view of Dmel\Dl 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
Comments on Gene Model
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0083739
5278
833
FBtr0083740
3546
833
FBtr0304658
4581
833
Additional Transcript Data and Comments
Reported size (kB)
5.4, 4.5, 3.6, 3.5, 2.8 (northern blot)
5.4, 4.6 (northern blot)
Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0083153
88.8
833
6.75
FBpp0083154
88.8
833
6.75
FBpp0293200
88.8
833
6.75
Polypeptides with Identical Sequences

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

833 aa isoforms: Dl-PA, Dl-PB, Dl-PC
Additional Polypeptide Data and Comments
Reported size (kDa)
Comments
Dl protein is used as a marker for the embryonic ventral large intestine.
It appears that Dl protein is targeted to the cell surface, but is efficiently removed by endocytosis, resulting in vesicular accumulation.
One of a couple of products generated by alternative splicing.
Dl protein has a similar structure to the N protein. Dl protein shares no significant homology to other proteins outside of the EGF repeats.
External Data
Subunit Structure (UniProtKB)
Interacts with N via the EGF repeats and the N EGF repeats.
(UniProt, P10041)
Post Translational Modification
Ubiquitinated by Mib, leading to its endocytosis and subsequent degradation.
(UniProt, P10041)
Linkouts
Sequences Consistent with the Gene Model
Nucleotide / Polypeptide Records
 
Mapped Features

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

External Data
Crossreferences
Linkouts
Gene Ontology (51 terms)
Molecular Function (5 terms)
Terms Based on Experimental Evidence (4 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from direct assay
inferred from physical interaction with FLYBASE:N; FB:FBgn0004647
inferred from physical interaction with UniProtKB:Q9VUX2
(assigned by UniProt )
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from electronic annotation with InterPro:IPR001881, InterPro:IPR018097
(assigned by InterPro )
inferred from biological aspect of ancestor with PANTHER:PTN002371879
(assigned by GO_Central )
Biological Process (36 terms)
Terms Based on Experimental Evidence (28 terms)
CV Term
Evidence
References
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
Terms Based on Predictions or Assertions (9 terms)
CV Term
Evidence
References
traceable author statement
traceable author statement
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN002372732
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN001170801
(assigned by GO_Central )
Cellular Component (10 terms)
Terms Based on Experimental Evidence (10 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN002372732
(assigned by GO_Central )
Expression Data
Expression Summary Ribbons
Colored tiles in ribbon indicate that expression data has been curated by FlyBase for that anatomical location. Colorless tiles indicate that there is no curated data for that location.
For complete stage-specific expression data, view the modENCODE Development RNA-Seq section under High-Throughput Expression below.
Transcript Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
organism

Comment: maternally deposited

dorsal ectoderm anlage

Comment: anlage in statu nascendi

ventral ectoderm anlage

Comment: anlage in statu nascendi

antennal anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

dorsal head epidermis anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

visual anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

antennal primordium

Comment: reported as procephalic ectoderm primordium

central brain primordium

Comment: reported as procephalic ectoderm primordium

visual primordium

Comment: reported as procephalic ectoderm primordium

dorsal head epidermis primordium

Comment: reported as procephalic ectoderm primordium

lateral head epidermis primordium

Comment: reported as procephalic ectoderm primordium

ventral head epidermis primordium

Comment: reported as procephalic ectoderm primordium

northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Excised Dl introns accumulate in two foci in the nucleus.
Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
distribution deduced from reporter
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Dl protein is present on myogenic cell membranes.
Expression of Dl is widespread in the mesoderm at embryonic stage 12. By the end of the period, it becomes restricted to cardioblasts. Based on cell size and shape and the expression levels of Dl, dorsal and ventral subdomains within the cardiogenic mesoderm of stage 12 embryos can be distinguished. Cells of the ventral domain are small and express moderate levels of Dl and tin. Dorsally, larger cells expressing higher levels of tin are observed. Dl expression is highly dynamic in the dorsal domain. At most timepoints during stage 12, anterior and posterior clusters of strongly Dl-positive cells are seen, flanking a central cluster with lower Dl levels. The central cluster expresses eve. eve expression defines a dorso-central cluster from which the pair of eve-positive pericardial cells is specified. The later eve-positive/low-Dl dorso-central cluster gives rise to a dorsal muscle. The anterior and posterior, high-Dl clusters form the definitive cardiogenic mesoderm. They will give rise to the cardioblasts of the dorsal vessel and the odd-positive blood progenitors and pericardial nephrocytes. The ventral domain showing low levels of tin and Dl contribute to the dorsal musculature. Individual lineages derived from the cardiogenic mesoderm segregate from each other and begin to differentiate during the second half of stage 12. The anterior and posterior high-Dl cluster of each segment move closer together, while the central, low-Dl cluster moves out of the way, migrating laterally and ventrally. Dl expression becomes restricted to the cardioblasts. In the thoracic segments, each of the high-Dl clusters forms two cardioblasts while in the abdominal segments, three cardioblasts arise per cluster. However, only two cells of each abdominal cluster maintain a high level of Dl and tin. The third cell down-regulates these genes and expresses svp. A pattern of alternating sets of four tin/Dl-positive and two svp-positive cardioblasts characteristic of the abdominal dorsal vessel is generated.
The expression of ey, ap, and Dll were compared in outer optic lobes (OPC) starting in late third instar larvae. At this stage they were expressed as three distinct cell populations. In anterior sections, the three genes are expressed a three parallele stripes of cells that represent rows of neurons that emerge from the OPC. They correspond to progeny from the youngest to oldest neuroblasts. In middle sections, Dll-positive cells are generated in the progeny of the oldest neuroblasts, with ey-positive and ap-positive cells often placed below Dll-positive (in cells that had emerged earlier from the these neuroblasts). By the beginning of pupation, the number of cells origination from the OPC increased. A major reorganization of optic lobe structure occurs around P20 such that the three stripes are no longer distinguishable and the three cell populations are extensively interspersed within the adult medulla cortex.
Dl protein is strongly expressed in neuroepithelial cells of the inner and outer optic anlagen (IPC, OPC) from late second to late third instar larval stages. In the OPC, Dl immunoreactivity is stronger in the medial neuroepithelial cells that border the medulla neuroblasts. Dl protein expression is detected at a lower level in medulla neuroblasts, but is higher in newly generated medulla neurons; however it is not detected in mature medulla neurons or their axons. Dl protein is weakly expressed in the lamina anlage, and in anterior cells in the lamina; it is more strongly expressed as punctate dots in posterior lamina cells.
Dl protein is observed primarily in intracellular vesicles in eye discs though some cytoplasmic staining is seen in cells within the morphogenetic furrow.
Dl protein is localized to the segment boundaries of all leg segments in leg discs.
Dl protein is expressed in presumptive wing veins in the wing disc.
Dl protein is expressed in the invaginating ectodermal cells of the keyhole structure of the developing embryonic proventriculus. Dl protein is downregulated in the anterior- and posterior-most cell rows of the keyhole structure after embryonic stage 15.
Dl is expressed along the ventral side of the DV boundary and along the longitudinal veins in the ventral compartment. Dl is not expressed in dorsal cells.
At embryonic stage 11, Dl protein expression is observed in cells surrounding the cells of visceral mesoderm, in particular in the cells surrounding the fusion-competent myoblasts.
Dl protein is rapidly internalized and is detected intracellularly in developing eye discs of third instar larvae.
Well defined staining of crossveins is observed by 23-26 hr APF.
Dl protein is expressed in all microchaeta proneural cells and microchaeta sensory organ precursors (SOPs) and is expressed dynamically in SOP progeny. Dl expression in microchaeta proneural cells is detected before ac expression.
Dl protein is first detected in cells in the morphogenetic furrow. It is primarily accumulated in vesicles located apically within each cell though some cytoplasmic staining is seen. After cells emerge from the furrow, Dl protein is localized exclusively to vesicles that are primarilly localized apically. In earlier rows, Dl protein accumulates in vesicles in R8, R2 and R5. Subsequently, Dl protein disappears from those cells and is seen only in R3 and R4 by row 5. Between rows 6 and 8, vesicles are also observed in R1 and R6 and three rows later, vesicles are apparent in R3, R4, R1, R6, and R7. Dl protein ceases to accumulate in R3, R1, and R6, but continues to be found in R4 and R7 until at least row 14.
Dl protein can be detected throughout oogenesis. It is first detected in the germarium where diffuse cytoplasmic staining and small bright vesicular staining is observed. In stages 1-3, diffuse cytoplasmic staining is again seen. Dl protein accumulates in vesicular features associated with the membranes of nurse cells and oocytes starting in stages 4-5. In stages 5-6, intense staining is observed at the junction between the follicle cells and the nurse cells and oocyte. Dl protein is also apparent in the membranes surrounding the ring canals. By stages 7-8, Dl protein levels fall to background at the membranes at the junction of the oocyte and follicle cells but remain high at the junctions of nurse cells and follicle cells. uring stages 9 and 10A, Dl protein accumulation becomes reduced in the follicle cell, nurse cell, and oocyte membranes and becomes more pronounced in vesicles. Starting in stage 10B-11, Dl protein appears to be transferred to the oocyte from the nurse cells. It is also expressed in a subset of centripetally migrating follicle cells. From stage 11 on, it is expressed at background levels throughout the follicle except at the nurse cell-oocyte border. N protein and Dl protein localization were compared during oogenesis. In the germarium, cytoplasmic N and Dl protein staining are observed. In contrast to Dl protein, more intense N staining is seen in the membranes of follicle cells in regions 2 and 3 of the germarium. Diffuse cytoplasmic staining of N and Dl proteins is bserved in stages 1-6. In contrast to Dl protein, follicle cell membrane staining of N protein is observed during this whole period. In stages 4-5, N and Dl protein accumulation is apically polarized within the membranes of all follicle cells but some N protein is also present in the basal membranes. N and Dl protein staining is also observed in nurse cell membranes and cytoplasm but the membrane staining is stronger for Dl protein than N protein. By stages 7-8, in contrast to Dl protein, N protein is still present in the membranes between oocytes and follicle cells. N protein is expressed in the membranes of all follicle cells that surround the egg chamber in stages 7-9. From stage 9, N protein accumulation decreases in follicle cell membranes but persists in urse cell membranes. N protein also accumulates in two specialized groups of follicle cells situated dorsolaterally at the nurse cell chamber-oocyte junction which eventually form the chorionic appendages. No Dl accumulation is seen in these cells. While Dl protein appears to be transferred from nurse cells to the oocyte during stage 11, N protein is not transferred.
Dl protein is first detected in the cortical membrane of precellular blastoderm embryos. Just before gastrulation, the level of Dl protein decreases in the presumptive mesoderm region of the embryo and profuse vesicular subcellular staining is observed. These vesicles are associated with endocytosis from the membrane. Dl protein is expressed in the ectodermal cells within the neurogenic region and in mesectodermal cells through the waves of neuroblast segregation. Dl protein is not apparent in the segregated neuroblasts but continues to be expressed in the developing epidermis. It is expressed transiently in the mesoderm at the end of neuroblast segregation and is also detected in the procephalic neurogenic region and withinndodermal derivatives including the anterior and posterior midgut invaginations and part of the hindgut. By stage 11, expression is mainly restricted to the developing epidermis and the posterior midgut. During germ band retraction, Dl protein is expressed in a number of tissues including what appears to be the primordia of the optic lobes, the stomatogastric nervous system or antennomaxillary complex, and the epiphysis. It is also expressed in the tracheal trunks, proventriculus, hindgut, pharynx, proesophageal ganglion, and anterior and posterior midguts. It\'s expression in the ventral nerve cord appears to be restricted to dividing cells both in the midline and in the CNS. In larvae, Dl expression is observed in a number of tissues. Dl protein is expressed in CNS neuroblasts andtheir progeny in all three larval instars and within the developing proliferation centers. It is also expressed in cells along the ventral midline that may be glial. In eye discs, Dl protein expression is first seen on the surfaces of unpatterned cells ahead of the morphogenetic furrow. It is then observed in clusters of cells in the morphogenetic furrow and extending behind the furrow. Expression appears to be restricted to apical vescicles (thought to be multivesicular bodies) near the center of each developing ommatidium. The Dl-expressing cells appear to include the photoreceptor cells. Later Dl protein is expressed in cone cells and in the peripodial membrane. Dl expression is also observed in the antennal portion of the eye-antennal disc. A complex pattern of Dl protein epression is described in the wing disc. Dl expression is observed in nearly all cells of the wing disc but at an elevated level in some areas. These include two bands of cells flanking the anterior wing margin that give rise to sensory organ precursors. Two bands of cells flanking the posterior wing margin also express elevated levels of dl protein and may give rise to non-innervated epidermal hairs. In the notum regions, cells that express elevated Dl protein levels appear to correspond to macrochaeta proneural groups. Six hours after puparium formation, Dl protein is expressed in regions where developing bristles are forming along the anterior wing margin, where epidermal hairs are forming along the posterior wing margin, and within the presumptive wing veins. Two groups of intnsely staining cells in the third longitudinal vein correspond to the developing campaniform sensilla. Finally Dl and N expression are compared in the larval CNS, wing discs, and eye-antennal discs.
Marker for
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GawB}Dl05151-G
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GawB}DlNP0677
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GMR24H06-GAL4}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}1282
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS049520
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS092611b
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS105314
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS111909
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS130403
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS142311
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS144011
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}DlS148011b
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lArB}DlA326.2F3
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{PZ}Dl05151
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\Dl in GBrowse 2
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
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
FlyExpress - Embryonic expression images (BDGP data)
  • Stages(s) 1-3
  • Stages(s) 4-6
  • Stages(s) 7-8
  • Stages(s) 9-10
  • Stages(s) 11-12
  • Stages(s) 13-16
Alleles, Insertions, and Transgenic Constructs
Classical and Insertion Alleles ( 350 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 80 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of Dl
Transgenic constructs containing regulatory region of Dl
Deletions and Duplications ( 26 )
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
abdominal tergite marginal bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
anterior notopleural bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
anterior postalar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
anterior scutellar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
anterior supraalar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
cell-cell adherens junction & dorsal mesothoracic disc, with Scer\GAL4Act5C.PI
embryonic/larval dorsal branch & tracheal tip cell
embryonic/larval dorsal trunk & tracheal tip cell, with Scer\GAL4btl.PS
eye disc & neuron
eye photoreceptor cell & eye disc | posterior, with Scer\GAL4sca-537.4
eye photoreceptor cell & ommatidium | ectopic
femur & joint, with Scer\GAL4klu-G410
filamentous actin & dorsal mesothoracic disc, with Scer\GAL4Act5C.PI
follicle cell & mitotic cell cycle | germ-line clone | cell non-autonomous
fusion competent cell & visceral mesoderm
interommatidial bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
macrochaeta & scutum
mesothoracic leg sensillum & trichogen cell, with Scer\GAL4l(3)31-1-31-1
mesothoracic tergum & macrochaeta, with Scer\GAL4sca-C253
mesothoracic tergum & sensory organ cell | ectopic, with Scer\GAL4Act5C.PI
metathoracic leg sensillum & trichogen cell, with Scer\GAL4l(3)31-1-31-1
microchaeta & adult thorax
microtubule & oocyte
muscle founder cell & visceral mesoderm
neuron & peripheral nervous system
oocyte & pericentriolar material, with Scer\GAL4hs.PB
posterior dorsocentral bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
posterior notopleural bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
posterior postalar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
posterior scutellar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
posterior supraalar bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
presutural bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
prothoracic leg sensillum & trichogen cell, with Scer\GAL4l(3)31-1-31-1
scutum & macrochaeta & trichogen cell, with Scer\GAL4l(3)31-1-31-1
scutum & macrochaeta | somatic clone
sensory mother cell & filopodium
sensory mother cell & filopodium, with Scer\GAL4neur-P72
sex comb & trichogen cell, with Scer\GAL4l(3)31-1-31-1
tarsal segment & joint, with Scer\GAL4klu-G410
thorax & macrochaeta
tibia & joint, with Scer\GAL4klu-G410
wing margin bristle & trichogen cell, with Scer\GAL4l(3)31-1-31-1
wing sensillum & trichogen cell, with Scer\GAL4l(3)31-1-31-1
Orthologs
Human Orthologs (via DIOPT v7.1)
Homo sapiens (Human) (6)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
13 of 15
Yes
Yes
10 of 15
No
Yes
2 of 15
No
Yes
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
Model Organism Orthologs (via DIOPT v7.1)
Mus musculus (laboratory mouse) (6)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
12 of 15
Yes
Yes
10 of 15
No
Yes
2 of 15
No
Yes
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Rattus norvegicus (Norway rat) (6)
9 of 13
Yes
Yes
7 of 13
No
Yes
2 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Xenopus tropicalis (Western clawed frog) (5)
12 of 12
Yes
Yes
5 of 12
No
Yes
5 of 12
No
Yes
1 of 12
No
No
1 of 12
No
Yes
Danio rerio (Zebrafish) (11)
12 of 15
Yes
Yes
10 of 15
No
Yes
9 of 15
No
Yes
9 of 15
No
Yes
8 of 15
No
Yes
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
Yes
Caenorhabditis elegans (Nematode, roundworm) (7)
3 of 15
Yes
Yes
2 of 15
No
Yes
2 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
Yes
1 of 15
No
Yes
Arabidopsis thaliana (thale-cress) (0)
No records found.
Saccharomyces cerevisiae (Brewer's yeast) (0)
No records found.
Schizosaccharomyces pombe (Fission yeast) (0)
No records found.
Orthologs in Drosophila Species (via OrthoDB v9.1) ( EOG091902GI )
Organism
Common Name
Gene
AAA Syntenic Ortholog
Multiple Dmel Genes in this Orthologous Group
Drosophila melanogaster
fruit fly
Drosophila suzukii
Spotted wing Drosophila
Drosophila simulans
Drosophila sechellia
Drosophila erecta
Drosophila yakuba
Drosophila ananassae
Drosophila pseudoobscura pseudoobscura
Drosophila persimilis
Drosophila willistoni
Drosophila virilis
Drosophila mojavensis
Drosophila grimshawi
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091501JF )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Musca domestica
House fly
Glossina morsitans
Tsetse fly
Lucilia cuprina
Australian sheep blowfly
Mayetiola destructor
Hessian fly
Aedes aegypti
Yellow fever mosquito
Anopheles gambiae
Malaria mosquito
Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( EOG090W033O )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Bombyx mori
Silkmoth
Danaus plexippus
Monarch butterfly
Heliconius melpomene
Postman butterfly
Apis florea
Little honeybee
Apis mellifera
Western honey bee
Bombus impatiens
Common eastern bumble bee
Bombus terrestris
Buff-tailed bumblebee
Linepithema humile
Argentine ant
Megachile rotundata
Alfalfa leafcutting bee
Nasonia vitripennis
Parasitic wasp
Dendroctonus ponderosae
Mountain pine beetle
Tribolium castaneum
Red flour beetle
Pediculus humanus
Human body louse
Rhodnius prolixus
Kissing bug
Cimex lectularius
Bed bug
Acyrthosiphon pisum
Pea aphid
Zootermopsis nevadensis
Nevada dampwood termite
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X02EX )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strigamia maritima
European centipede
Ixodes scapularis
Black-legged tick
Stegodyphus mimosarum
African social velvet spider
Stegodyphus mimosarum
African social velvet spider
Tetranychus urticae
Two-spotted spider mite
Daphnia pulex
Water flea
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( EOG091G07YQ )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strongylocentrotus purpuratus
Purple sea urchin
Ciona intestinalis
Vase tunicate
Gallus gallus
Domestic chicken
Gallus gallus
Domestic chicken
Paralogs
Paralogs (via DIOPT v7.1)
Drosophila melanogaster (Fruit fly) (7)
3 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Model Summary Ribbon
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 2 )
Potential Models Based on Orthology ( 0 )
Human Ortholog
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 4 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease Associations of Human Orthologs (via DIOPT v7.1 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Homo sapiens (Human)
Gene name
Score
OMIM
OMIM Phenotype
DO term
Complementation?
Transgene?
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
esyN Network Diagram
Show neighbor-neighbor interactions:
Select Layout:
Legend:
Protein
RNA
Selected Interactor(s)
Interactions Browser

Please see the Physical Interaction reports below for full details
RNA-RNA
Physical Interaction
Assay
References
protein-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
esyN Network Diagram
esyN Network Key:
Suppression
Enhancement

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
enhanceable
External Data
Subunit Structure (UniProtKB)
Interacts with N via the EGF repeats and the N EGF repeats.
(UniProt, P10041 )
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Gene Group - Pathway Membership (FlyBase)
Notch Signaling Pathway Core Components -
The Notch receptor signaling pathway is activated by the binding of the transmembrane receptor Notch (N) to transmembrane ligands, Dl or Ser, presented on adjacent cells. This results in the proteolytic cleavage of N, releasing the intracellular domain (NICD). NICD translocates into the nucleus, interacting with Su(H) and mam to form a transcription complex, which up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0225731 and FBrf0192604). Core pathway components are required for signaling from the sending cell and response in the receiving cell.
External Data
Linkouts
KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Genomic Location and Detailed Mapping Data
Chromosome (arm)
3R
Recombination map
3-66
Cytogenetic map
Sequence location
3R:19,302,731..19,326,217 [-]
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
92A1-92A2
Limits computationally determined from genome sequence between P{EP}EP650 and P{PZ}l(3)1058510585
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
92A1-92A2
(determined by in situ hybridisation)
92A-92A
(determined by in situ hybridisation)
92A2-92A2
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Left of (cM)
Right of (cM)
Notes
Stocks and Reagents
Stocks (68)
Genomic Clones (38)
cDNA Clones (162)
 

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 GBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequences
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)
    RNAi and Array Information
    Linkouts
    DRSC - Results frm RNAi screens
    GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
    Antibody Information
    Laboratory Generated Antibodies
    Commercially Available Antibodies
     
    Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
    Other Information
    Relationship to Other Genes
    Source for database identify of
    Source for database merge of
    Source for merge of: Dl anon-WO0118547.269
    Additional comments
    Source for merge of Dl anon-WO0118547.269 was sequence comparison ( date:051113 ).
    Other Comments
    Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
    Ubiquitylation of the Dl intracellular domain seems to be a necessary step in the activation of N.
    Dl is ubiquitylated by neur and mib1.
    The Dl intracellular domain regulates the rate of Dl internalization and motif i2, the mib1 interaction motif, is critical for efficient internalization.
    Dl is required in the anterior polar follicle cells to form the stalk that connects adjacent egg chambers.
    The N signaling pathway is important for the formation and maintenance of the germline stem cell niche in the ovary.
    Dl signalling induces the anterior polar follicle cells of the egg chamber to signal through the JAK/STAT pathway and induce the formation of the interfollicle cell (or stalk) between adjacent egg chambers. This stalk formation is necessary for polarization of adjacent younger egg chambers by inducing the shape change and preferential adhesion that positions the oocyte at the posterior.
    Area matching Drosophila EST AA539491.
    Dl signals twice from the germ cells to control the timing of follicle cell differentiation.
    Dl has a role in leg and antennal segmentation.
    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.
    EGF-like repeats 11 and 12, the RAM-23 and cdc10/ankyrin repeats and the region C-terminal to the cdc10/ankyrin repeats of the N protein are necessary for both Dl and Ser proteins to signal via N. Dl and Ser utilise EGF-like repeats 24-26 of N for signalling, but there are significant differences in the way they utilise these repeats.
    Endocytosis of the ligand Dl, complexed with the N extracellular domain, into signal-generating cells is required for separation of the N extracellular domain from the N intracellular domain.
    Dl transcription in the early R3/R4 photoreceptor precursor cells is deregulated by Jra or hep activation.
    N protein responds differently to binding by Dl or wg protein. The Dl signal is transduced by the N intracellular domain released from the plasma membrane, the wg signal is transduced by the N intracellular domain associated with the plasma membrane.
    The composite signalling of the Ser and Dl genes through N patterns the segments of the leg, leading to the development of leg joints. Elsewhere in the tarsal segments, signalling by Dl and N is necessary for the development of non-joint parts of the leg.
    Dl-mediated activation of N is required for establishment of ommatidial polarity; N signaling induces the R4 fate.
    In cultured cells, heterotypic interactions between N protein and the ligands Dl and Ser have higher affinities than homotypic interactions between Dl protein molecules.
    Dl may activate N to specify cell fates at the tip of the developing tracheal branches.
    Candidate gene for quantitative trait (QTL) locus determining bristle number.
    The Dl ligand is cleaved at the cell surface, releasing an extracellular fragment capable of binding to N and acting as an antagonist of N activity. The kuz metalloprotease is required for this processing event.
    Local activation of N is necessary and sufficient to promote the formation of joints between segments of the leg. This segmentation process requires the participation of Ser, Dl and fng.
    In the developing trachea the selection of single fusion cells from the dpp responsive cells is accomplished by the up-regulation of the Dl ligand in the presumptive fusion cells and the activation of the N receptor in the cells that remain at the stalk of the branch.
    Eight EMS-induced alleles have been isolated that suppress the wing vein phenotypes of NAx-16, and the lethality of NAx-9/NAx-E2.
    Localization studies suggest that the relative levels of Su(H), Dl and N regulate nuclear entry of the N/Su(H) complex.
    Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit neurogenic pattern defects.
    Dl and Ser are redundant N signals required for asymmetric cell divisions within the sensory organ lineage.
    Genetic combinations with mutants of nub cause additive phenotypes.
    Dominant interactions indicate that toc is acting in the same signalling pathways for the formation of the egg chamber as da, N and Dl.
    The activities of Ser and Dl during wing development are studied.
    wg is required indirectly for ct expression, results suggest this requirement is due to the regulation by wg of Dl and Ser expression in cells flanking the ct and wg expression domains. Dl and Ser play a dual role in the regulation of ct and wg expression.
    Ser and Dl maintain each other's expression in the wing by a positive feedback loop. fng functions to position and restrict this feedback loop to the developing dorsal-ventral boundary.
    Dl is transcribed and translated in a dynamic pattern during microchaetae sensory organ precursor (SOP) specification and subsequent bristle development. Neurogenic signalling is required at each step of bristle development for correct cell fate specification. The regulatory relationship between the N-Dl signalling pathway and the proneural genes ac and sc during early microchaetae development is assayed.
    3 alleles of Dl have been isolated in a genetic screen for autosomal mutations that produce blisters in somatic wing clones.
    Segregation of neuroblasts is studied in mutant and rescued flies to study the role of transcriptional regulation of Dl.
    The secreted forms of the Dl and Ser gene products are antagonists of N signalling in the developing eye and wing.
    The combined effect of N and its target genes ct and wg regulate the expression of N ligands Dl and Ser which restrict N signalling to the wing dorsoventral boundary.
    Study of expression and function of different components of the N pathway in both the wing disc and pupal wings proposes that the establishment of vein thickness utilises a combination of mechanisms. These include: independent regulation of N and Dl expression in intervein and vein territories, N activation by Dl in cells where N and Dl expression overlaps, positive feedback on N transcription in cells where N has been activated and repression of rho transcription by HLHmβ and maintenance of Dl expression by rho/Egfr activity.
    dsh interacts antagonistically with N and Dl. A physical interaction of the dsh product with the carboxy terminus of that of N suggests a basis for the interaction. Thus dsh, in addition to transducing wg signal, blocks N signalling directly, explaining the inhibitory cross talk observed between the pathways.
    N-expressing cells in a given compartment have different responses to Dl and Ser. Dl and Ser function as compartment-specific signals in the wing disc, to activate N and induce downstream genes required for wing formation.
    Proneural and neurogenic genes control specification and morphogenesis of stomatogastric nerve cell precursors.
    Dl and Ser have clearly distinct capabilities when ectopically expressed during wing development; Dl always acts as a strong activator of N and induces wing outgrowth and margin formation, Ser mediates activation of N only under certain circumstances and even acts as an inhibitor of N under other conditions.
    Immunoprecipitation assay, cell binding assays and cell aggregation assays demonstrate there is no interaction between sca and N (or Dl) proteins.
    Mutations show strong interactions with high and low selection lines, abdominal and sternopleural bristle numbers are affected. Results suggest Dl is a candidate for bristle number quantitative trait loci (QTL) in natural populations or is in the same genetic pathway.
    numb is not required to specify dMP2 fate, but that dMP2 fate is due to lack of productive Dl-N signaling. The function of numb is to antagonise the Dl-N signal specifying vMP2 fate. dMP2 and vMP2 neurons express N and adjacent cells express Dl.
    Intracellularly truncated forms of Ser and Dl behave as dominant-negative proteins in an apparently non-cell autonomous manner. The presence of intracellular domains is essential for proper N ligand function in the eye.
    Ser and Dl, two N ligands, have asymmetrical requirements at the dorsal-ventral boundary during wing development.
    Ser can replace Dl gene function during embryonic neuroblast segregation and expression of Ser leads to N-dependent suppression of ac expression in proneural clusters. Results suggest that Ser functions as an alternative ligand capable of N activation.
    fs(1)Yb is required in the soma for ovary follicle cell differentiation and to support later stages of egg maturation. Mutations at fs(1)Yb show genetic interactions with the N group of neurogenic genes.
    Ectopic expression of both rho and Dl in a mutant net background produces ectopic veins of normal thickness. Ectopic expression of rho alone produces whole intervein sectors converted into vein. The pattern of normal+ectopic wing veins resembles wing vein patterns of other flies with more veins than Drosophila.
    Neurogenic genes are not required for the organization of the principle midgut epithelial cells into an epithelium once the principle midgut epithelial cells are specified.
    Mutations can act as dominant modifiers of the activated N eye phenotype (FBrf0064452).
    Su(H) shows allele specific interactions with N, Dl, dx and mam. In cultured Drosophila cells, the Su(H) product is sequestered in the cytoplasm when coexpressed with N protein and is translocated to the nucleus when N protein binds its Dl protein ligand.
    Proneural gene products (ac, da and l(1)sc) activate transcription of Dl in the neuroectoderm by binding to specific sites within its promoter. This transcriptional activation enhances lateral inhibition and helps ensure that cells in the vicinity of prospective neuroblasts will themselves become epidermoblasts.
    Mutation in Dl affects sensory organ precursor formation.
    Dl is required for PNS development in the embryo.
    Genetic and phenotypic analysis suggests that the Abruptex class of N mutations cause stronger than normal N activation by the Dl product. The phenotypes of the Abruptex class of N allele are modified by mutations at Ser, Dl, H and gro.
    The expression patterns of N and Dl are highly regulated both spatially and temporally, and are similar, though do not coincide directly during a number of stages of oogenesis.
    Dl is a neurogenic gene required initially to ensure the correct number of PNS precursors. Dl is not required for the late epidermal maintenance function.
    Growth of axons in the intersegmental nerve is guided, in part by the products of Notch and Delta. Expression of Delta on a branch of the trachea provides a path, and the axons use the N protein on their surfaces to recognise the path. A similar mechanism specifies the trajectory of part of the axonal scaffold of the CNS.
    In addition to the binding of Notch molecules on one cell to the Delta molecules of opposing cells, the Notch and Delta proteins on the surface of the same cell may interact, altering the availability of these proteins to interact with their counterparts on adjacent cells.
    Multiphasic expression in the derivatives of many germ layers implies successive requirements for Delta function in a number of tissues. Notch and Delta expression are generally coincident within developing tissues. At the subcellular level, Delta and Notch are localized in endocytic vesicles during down regulation from the surfaces of interacting cells, consistent with their roles as signal and receptor.
    Dl function is required for the specification of the correct number of sensory mother cells, perhaps via a mutual inhibition mechanism, and acts during the latter stage of bristle organ morphogenesis to ensure establishment of neuronal and nonneuronal cell fates.
    Dl gene product is required during the third larval instar for completion of pupation, reduced Dl levels lead to macrochaetae multiplication, reduction eye size, eye scarring, ocellar fusion, tarsal segment deletion and wing notching. Dl gene product is also required during the pupal development for eclosion, reduced Dl levels lead to microchaetae multiplication and loss, interommatidial bristle multiplication and loss and eye glossiness.
    Analysis of deficiencies reveals that N and Dl are required for migration of the endoderm and its transition to an epithelium, though the anterior and posterior midgut primordia do express midgut-specific genes and the visceral mesoderm develops.
    A new allele of Notch, NM1, has been isolated that behaves genetically as both an antimorph and a loss of function allele: the basis for the antimorphism may lie in the titration of Delta products into non-functional ligand-receptor complexes. Genetic interactions with Delta and Serrate alleles of the Beaded locus suggest that NM1 products have modified binding abilities with both Dl and Bd products.
    The embryonic phenotype of neurogenic mutations was examined in most tissues using Ecol\lacZ enhancer trap lines. All alleles examined show defects in many organs from all three germ layers. At least for ectodermally and endodermally derived tissues, neurogenic gene function is primarily involved in interactions among cells that need to acquire or maintain an epithelial phenotype. A deficiency for Dl shows defects in neuroblasts, sensillum precursors, sensory neurons, optic lobe, somatogastric nervous system, Malpighian tubules, trachea, endoderm, larval midgut, somatic musculature, cardioblasts, and peritracheal and periligament cells. The salivary gland and foregut are totally and partially absent, respectively.
    Screens for Dominant enhancers or suppressors of the wing phenotype associated with Dl9P and DlFE32 identified mutations in 22 loci including Star, Hairless, Plexate, blistered, plexus and Nicked.
    All genomic Dl DNA that hybridises to minor Dl transcripts maps to the introns: introns excised from Dl shown by high resolution in situ hybridisations to whole mounts of embryos to localise to 2 foci/nucleus. Number of foci can be varied by altering the number of copies of the Dl gene. Larval and imaginal disc nuclei, where the chromosomes are paired, only have one focus. Excised introns do not diffuse away from foci til late prophase, when foci disperse into numerous small dots of hybridisation, suggesting that introns are associated with a structural element in the nucleus that is dissociated during cell division.
    Double mutant combinations reveal suppressive interactions with mutations at the H locus.
    Dl acts as the signal that passes on the lateral inhibitory signal from one cell to another via its physical interaction with the receptor trans-membrane protein N (Heitzler, Cell 64: 1083--1092).
    Dl is needed for proper mesoderm differentiation prior to the onset of nau expression: mutant alleles cause hypertrophy in nau expressing cells.
    Genetic analysis demonstrates that Dl, neu, E(spl), HLHm5, HLHm7 and m4 are functionally related. Spatial distribution of mRNA in neurogenic mutant embryos suggests that some of the functional interactions take place at the transcriptional level.
    Ecol\lacZ reporter gene constructs demonstrate that neurogenic loci are required to restrict the number of competent cells that will become sensory mother cells, SMCs.
    Dl is only required in cells expressing ac and sc.
    Dl is a trans-acting gene of the ASC. emcD shows mutual rescuing with Dl alleles.
    The mutant Dl phenotypes are likely to result from perturbation of neurogenic gene function in the germ cells.
    Dl is required for the singularization of sensory organ mother cells in chaetogenic regions and subsequent chaeta differentiation. Lack-of-function alleles of Dl exaggerate ASC "Hw" phenotypes in both ectopic and normal positions.
    Dl acts as a suppressor of spl alleles of N.
    Mutations in Dl cause thickened veins.
    An in vitro aggregation assay demonstrates that expression and interaction of N and Dl in cultured cells causes cell aggregation, this aggregation is calcium-dependent.
    Transcriptional organization of the Dl locus and the spatial pattern of mRNA accumulation during embryogenesis has been determined.
    Normal functioning of Dl+ ensures a correct differentiation between neural and epidermal cells.
    An extra wild type copy of Dl, in combination with dxENU, causes some pupal lethality, escapers have small eyes.
    Analysis of N and Dl mutant combinations reveals that reduction of the wild type number of Dl was capable of interferring with the mechanism underlying negative complementation in a manner that was not restricted to specific Abruptex combinations.
    Molecular analysis of Dl reveals that it has a transcriptionally complex locus that yields multiple maternal and zygotic transcripts. Genetic analysis demonstrates that Dl mutations can modify the imaginal phenotypes that result from heterozygosity for E(spl) and N mutations.
    In the loss-of-function alleles of tkv, N and Dl, thickened veins and occasional plexi are seen, associated with small wings. In the gain-of-function alleles the reciprocal phenotype is seen, associated with large wings. The Notch phenotypic group includes neurogenetic mutations involved in cell communications. Some alleles are embryonic lethal.
    Dl transcripts are present in derivatives of all three germ layers of the embryo. The spatial and temporal accumulation patterns of Dl transcripts may act pleiotropically during embryogenesis.
    Dl is a modifier of the spl-E(spl)1 interaction. N, Dl and E(spl) gene products interact directly during embryonic and imaginal development. Morphogenesis of the ectodermally derived adult eye is sensitive to the combined action of the N, Dl and E(spl) gene products.
    A study of the interactions between N, Dl, H and E(spl) suggest that the effects of H, Dl and E(spl) on N are allele specific and occurring at the protein level.
    Neural hyperplasia, caused by mutations in Dl, can be prevented by the presence of another neurogenic mutation in the same genome.
    Characterization of Dl transcript organization and gene expression reveals that the Dl locus encodes multiple transcripts.
    Increasing the gene dosage of Dl increases the severity of N- and neur- phenotypes. Increasing number of wild type copies of Dl does not modify the bib phenotype.
    Dl has been molecularly cloned and genetically characterized.
    Temporal and spatial expression patterns and the deduced protein structure encoded by Dl support the contention that Dl provides the specificity required for the regulatory signal mediating epidermogenesis.
    The expression of genes controlling neurogenesis is dependent on the previous activity of the genes controlling the development of the embryonic dorsal-ventral pattern.
    A haplo-insufficient member of the group of neurogenic genes originally described on the basis of its dominant phenotype. Several classes of alleles designated by Vassin and Campos-Ortega based on the phenotype of heterozygous adults: Amorphic and strong hypomorphic alleles display wing veins widened at their junctions with the margin to form δ-like structures; in addition, they show irregular thickening of vein 2 and wings frequently held in divergent attitude; fusion of ommatidia may give rise to disruptions in regular hexagonal array of eye facets; ocelli are slightly enlarged; additional bristles are present on head, thorax, and abdomen; homozygotes die as embryos. Rare antimorphic alleles display the above phenotype in exaggerated form with irregular widening of all longitudinal wing veins, enlarged deltas, regularly divergent wings, smaller rougher eyes, larger and often fused ocelli and further increase in the numbers of extra bristles; in addition, tarsal joints 2 to 4, but not 5 are fused; homozygotes are embryonic lethals. Rare recessive alleles show low levels of survival as homozygotes or transheterozygotes with more severe alleles; survivors usually display a less extreme version of the phenotype exhibited by heterozygotes for amorphic alleles; however, some combinations are wild type in appearance and others (e.g., the antimorphs) are lethal. The embryonic lethality of homozygotes displays the typical neurogenic phenotype with neural hyperplasia accompanied by epidermal aplasia; most or all cells of the neurogenic ectoderm recruited into the neurogenic pathway. Transplantation of homozygous Dl pole cells demonstrate Dl expression during oogenesis (Dietrich and Campos-Ortega, 1984). Dl classed as non-autonomous in that single cells from the neurogenic ectoderm of Dl- embryos are capable of giving rise to both neural and epidermal derivatives when transplanted into the neurogenic region of wild-type embryos, suggesting that Dl- cells are capable of responding normally to information from neighboring cells (Technau and Campos-Ortega, 1987). Transcription in cellular blastoderm seen in the ventrolateral neurogenic ectoderm, with a ventral-to-dorsal gradient of expression, corresponding to the gradient of neurogenic capabilities of the neurogenic ectoderm. During gastrulation a metameric pattern of expression appears, disappears and reappears; as development proceeds complicated spatial and temporal specificities of expression ensue (Vassin, Bremer, Knust and Campos-Ortega, 1987). Interactions with other neurogenic mutations complex; Dl mutations suppress the spl-enhancing effect of E(spl) (Shepard, Boverman, and Muskavitch, 1988) and the expression of Ax (Siren and Portin, 1989); severe alleles fail to survive in heterozygotes with E(spl) loss-of-function alleles (Lehmann, Dietrich, Jimenez and Campos-Ortega, 1981) especially when E(spl) is maternally inherited. Expression of Dl/+ observed to be partially suppressed by duplications for E(spl)+ (Vassin, Vielmetter and Campos-Ortega, 1985), yet, de la Concha, Dietrich, Weigel and Campos-Ortega (1988) report that extra doses of E(spl)+ enhance the neurogenic phenotype of Dl-. Dl/+ and Dl- phenotypes are suppressed by heterozygous and homozygous deficiencies for H, respectively. For example, H2 is able to suppress the phenotypic effects of Dl9P, either in Dl9P/+ or in Dl9P/Dl9P genotypes; Dl9P/Dl9P is cell lethal in both the eye and the cuticle; Dl9P H2/Dl9P H2 cells, on the other hand, develop nearly normally (Dietrich and Campos-Ortega, 1984). Expression of Dl enhanced by duplications for N+ or H+ and three doses of Dl+ enhance expression of N- and neu-, but reduce the severity of the mam- phenotype. de la Concha et al. (1988) have incorporated many of these observations into a model of neurogenic-gene interaction. Dl alleles interact synergistically with certain Minutes, producing extreme phenotypes and drastically lowered viability (Schultz, 1929); DlOf enhances svspa-Cat (Tsukamoto, 1956).
    Origin and Etymology
    Discoverer
    Etymology
    Identification
    External Crossreferences and Linkouts ( 378 )
    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 Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
    RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
    UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
    UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
    Other crossreferences
    BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
    Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
    Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
    Flygut - An atlas of the Drosophila adult midgut
    GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
    iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
    KEGG Genes - Molecular building blocks of life in the genomic space.
    KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
    modMine - A data warehouse for the modENCODE project
    Reactome - An open-source, open access, manually curated and peer-reviewed pathway database.
    SignaLink - A signaling pathway resource with multi-layered regulatory networks.
    Linkouts
    BioGRID - A database of protein and genetic interactions.
    DroID - A comprehensive database of gene and protein interactions.
    DRSC - Results frm RNAi screens
    Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
    FLIGHT - Cell culture data for RNAi and other high-throughput technologies
    FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
    FlyMine - An integrated database for Drosophila genomics
    Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
    InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
    KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
    MIST (genetic) - An integrated Molecular Interaction Database
    MIST (protein-protein) - An integrated Molecular Interaction Database
    Reactome - An open-source, open access, manually curated and peer-reviewed pathway database.
    Synonyms and Secondary IDs (27)
    Reported As
    Symbol Synonym
    Dl
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    anon-WO0118547.269
    l(3)05151
    l(3)92Ab
    l(3)j8C3