Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
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.
Interacts with N via the EGF repeats and the N EGF repeats.
Ubiquitinated by Mib, leading to its endocytosis and subsequent degradation.
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.
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
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 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.
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.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Dl in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
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.
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
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.
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.
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.
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.
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.
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.
Genetic combinations with mutants of nub cause additive phenotypes.
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.
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.
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.
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 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.
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.
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.
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.
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.
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.
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).