Bd, Rpw, Beaded
transmembrane - EGF homolog - ligand for Notch - involved in the induction, through Notch, of the wing margin at the dorsal-ventral interface of the wing imaginal disc - a Serrate-Notch-Canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development.
Gene model reviewed during 5.53
Low-frequency RNA-Seq exon junction(s) not annotated.
If the first AUG is used, the protein is 1443aa. The second AUG has a better match to the Cavener consensus.
Ubiquitinated by mind-bomb, 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\Ser using the Feature Mapper tool.
Ser is expressed at both sides of the DV boundary and along the longitudinal veins.
During the third larval instar, the expression of Ser protein is re- solved into a complex pattern that includes two stripes of expression dorsal and ventral to the wing margin and ex- pression domains on the ventral and dorsal wing blades, including prospective wing veins 3–5.
Ser protein is first observed in stage 11 embryos in the clypeolabrum anlage and later in the hypopharyngeal lobe. These regions later form the roof and floor of the pharynx. In late stage 11, expression is observed in a ring of cells surrounding the stomodeum which come to lie in the anterior part of the proventriculus. Beginning in stage 11, a metameric pattern of expression is seen in the epidermis. Expression is also observed in the gnathal segments and in the anlage of the anal pads. From stage 12 onward, two defined regions of expression are apparent in the hindgut . From stage 13 onward, expression is observed in the two main lateral trunks of the tracheal system and in the anterior and posterior spiracles. Expression is detected in the secretory ducts of the salivary glands and on the ventral side of the frontal sac from stage 14 onward. Finally, from stage 15 onward, expression is observed in the anterior and posterior commissures of each segment as well as in the roots of the segmental nerves and in some axons in the brain. In wing imaginal discs, expression is observed in a row of cells located across the wing pouch, in three stripes perpendicular to it, and in some regions at the border of the wing disc. These regions correspond to the future wing margin and anlage of the alula.
Comment: in cells abutting the boundary
Comment: in cells abutting the boundary
GBrowse - Visual display of RNA-Seq signalsView Dmel\Ser 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.
May be allelic to Ndw.
One of 42 Drosophila genes identified as being most likely to reveal molecular and cellular mechanisms of nervous system development or plasticity relevant to human Mental Retardation disorders.
A Ser expressing signalling centre in the lymph gland may control haematopoiesis.
Ser is a strong candidate for the peripodial to columnar signal demonstrated to be important in eye development.
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.
Candidate gene for quantitative trait locus.
Ser is required for the normal morphogenesis of the abdominal denticle belts and maxillary mouth hooks in the embryo.
Ser is not required for the initiation of wing development, but rather for the expansion and early patterning of the wing primordium.
ap mediates cell interactions across the DV axis of the wing by regulating the expression of Ser and fng. In ap mutants the wing is lost, this phenotype can be rescued by ectopic expression of either Ser or fng and the resulting wings have both dorsal and ventral cell fates.
Genetic combinations with mutants of nub cause additive phenotypes.
Ser does not signal in the dorsal regions of the developing imaginal wing disc due to the action of the fng gene product. Ectopic expression studies reveal the regulation of Ser by fng occurs at the level of protein and not Ser transcription.
The activities of Ser and Dl during wing development are studied. Ser can activate or inactivate N in a concentration-dependent manner. While inactivation is likely to be mediated by a dominant negative effect over N, the activation is similar to that elicited by Dl and requires the product of the Su(H) gene. Results indicate that regulation of the concentration of Ser during development must be an important way of regulating its activity.
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.
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.
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.
Ser activity is not essential for proper eye development. 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.
Induction of vg requires the combined activities of Ser, wg and N. Based on the patterns of expression and requirements for Ser and wg during initiation wing development it is proposed that Ser is a dorsal signal and that wg is a ventral signal. Their combination at the dorso-ventral interface activates the N receptor and leads to vg expression.
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.
Compartmentalization of the wing disc, dorsal cell behaviour and the expression of two dorsally expressed putative signalling molecules, fng and Ser, are regulated by the ap selector gene. fng and Ser are distinct components of a single ap-regulated cell recognition and signal induction mechanism. Clonal analysis demonstrates that fng serves as a boundary-determining molecule such that Ser is induced wherever cells expressing fng and cells not expressing fng are juxtaposed.
Wild type function of Ser is required for the control of position-specific cell proliferation during development of meso- and metathoracic dorsal discs, which in turn exerts a direct effect on morphogenesis.
A new allele of Notch, NM1, has been isolated that behaves genetically as both an antimorph and a loss of function allele: 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 dominant Ser mutation causes a gap in the posterior wing tip and margin and a portion of the blade. The phenotype of homozygous Ser flies ranges from deep incisions of the wing to gaps in the wing margin. Ser is a wing margin mutation that interacts synergistically with ct. Double mutants with ct46l and ct53d have extreme phenotypes and suffer tissue loss at the wing tip which is not seen in the single mutants. Ser has no effect on ctL32 mutants as they have already lost the wing tip tissue.
Analysis of mosaic females indicates that Ser, ea, snk and tub are expressed in the germline during oogenesis.
Phenotypic interactions of Ser alleles with the neurogenic mutations in N and Dl together with the structural similarity of the proteins encoded by the genes suggest close interactions at the protein level.
Ser is an essential EGF-like protein.
Mutant individuals display notched wing tips.
"Maps to the right of ro: 2.1" was stated as revision. "Maps to the right of Pr: 1.5" was stated as revision.
Originally recovered alleles were recessive lethal with a dominant incised-wing phenotype; SerBd-1 was very weak and highly variable when first recovered, but gained expressivity with selection; subsequently isolated alleles were stronger. Wings reduced by marginal excision both anteriorly and posteriorly. Phenotype of SerBd-1/SerBd-1/+ extreme (Peter Lewis). Expression and interaction studied by Goldschmidt and Gardner (1942). Expression of SerBd-1, SerBd-3 and Ser1 suppressed by H (Bridges, 1938) and Ax alleles (Bang). In combination with several different Minutes, causes incomplete development of anal and genital imaginal discs in males and less frequently in females (Goldschmidt, 1948; Sturtevant, 1949). Ser1 (originally designated Ser: Serrate) homozygous viable; initially thought to be homozygous lethal, but lethality removable by recombination (Belt, 1971). The closely linked recessive lethal persists in many Ser1-bearing chromosomes. Recessive lethal alleles, which lack the dominant wing phenotype, recovered as revertants of Ser1 (symbolized "SerSrv") or selected on the basis of their failure to complement the lethality of SerBd-3 (symbolized Bdr). Allelism of SerBd-r1 (originally designated std: serratoid) inferred from enhanced wing incising in heterozygotes with Ser1 and genetic map position similar to that of Ser1; homozygous viability unknown. Cuticle preparations of embryos homozygous for Ser1 revertants reveal lack of germband retraction, improper deposition of cuticle, lack of head and thoracic structures, lack of Filzkorper and in severe cases, only a remaining patch of cuticle (either ventral or dorsal). Central-nervous-system defects revealed by anti-horseradish peroxidase preparations include breaks in the longitudinal and/or commissure nerve tracts, twisted or unretracted nerve tracts, only a single nerve tract and occasionally only the presence of groups of staining cells scattered throughout the embryo (Fleming et al., 1990). Each "SerSrv" allele displays the whole range of embryonic phenotypes but the proportions of individuals with a particular phenotype varies between alleles.