The gene Serrate is referred to in FlyBase by the symbol Dmel\Ser (CG6127, FBgn0004197). It is a protein_coding_gene from Drosophila melanogaster. There is experimental evidence that it has the molecular function: Notch binding; protein binding. There is experimental evidence for 14 unique biological process terms, many of which group under: single-organism developmental process; biological regulation; system development; cellular process; gland morphogenesis; post-embryonic organ morphogenesis; sensory organ development; immune system process; salivary gland morphogenesis; cell fate commitment. 82 alleles are reported. The phenotypes of these alleles are annotated with: adult segment; organ system subdivision; organ system; external compound sense organ; cephalopharyngeal skeleton; imaginal precursor; appendage segment; cell part; spiracle; integumentary specialisation. It has one annotated transcript and one annotated polypeptide. Protein features are: Delta/Serrate/lag-2 (DSL) protein; EGF-like calcium-binding; EGF-like calcium-binding, conserved site; EGF-like, conserved site; EGF-type aspartate/asparagine hydroxylation site; Epidermal growth factor-like domain; Jagged/Serrate protein; Notch ligand, N-terminal; VWC out. Summary of modENCODE Temporal Expression Profile: Temporal profile ranges from a peak of moderately high expression to a trough of extremely low expression. Peak expression observed within 06-18 hour embryonic stages, at stages throughout the pupal period. Summary of FlyAtlas Anatomical Expression Data: Expression at moderate levels in the following post-embryonic organs or tissues: adult hindgut, larval trachea. Comments on Affy2 ProbeSet: ProbeSet 1634766_at completely aligns to an exonic region of the only FlyBase-annotated transcript isoform of Ser. Gene sequence location is 3R:22997818..23019716.
User Contributed Data
Phenotypic Description from the Red Book (Lindsley
& Zimm 1992)
Gene/Allele symbols may differ
from current usage
From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ.
No. 327: 152.
Originally recovered alleles were recessive lethal
with a dominant incised-wing phenotype; Bd1 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 Bd1/Bd1/+ extreme (Peter Lewis).
Expression and interaction studied by Goldschmidt and Gardner
[1942, Univ. Calif. (Berkeley) Publ. Zool. 49: 103-24].
Expression of Bd1, Bd3, and BdS suppressed by H (DIS 9) 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, Proc. Nat. Acad. Sci. USA 34: 245-52;
Sturtevant, 1949, Proc. Nat. Acad. Sci. USA 35: 311-13). BdS
(originally designated Ser: Serrate) homozygous viable; initially thought to be homozygous lethal, but lethality removable by recombination (Belt, 1971, DIS 46: 116). The closely
linked recessive lethal persists in many BdS-bearing chromosomes. Recessive lethal alleles, which lack the dominant wing
phenotype, recovered as revertants of BdS (symbolized BdSrv)
or selected on the basis of their failure to complement the
lethality of Bd3 (symbolized Bdr). Allelism of Bdr1 (originally designated std: serratoid) inferred from enhanced wing
incising in heterozygotes with BdS and genetic map position
similar to that of BdS; homozygous viability unknown. Cuticle
preparations of embryos homozygous for BdS 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.). Each BdSrv
allele displays the whole range of embryonic phenotypes but
the proportions of individuals with a particular phenotype
varies between alleles.
Edith M. Wallace, unpublished.
Wings of BdS/+ and BdS/Df(3R)Ser notched at tip;
deepest notch at second posterior cell. In triploids, one
dose of BdS overlaps wild type. BdS is homozygous viable;
initially thought to be homozygous lethal, but lethality
removable by recombination (Belt, 1971, DIS 46: 116); the
closely linked recessive lethal persists in many BdS-bearing
chromosomes. Homozygous BdS produces extreme incision of wing
margins especially in second posterior cell (Belt, 1971). As
with other Bd alleles expression suppressed by H and Ax
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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.
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.
Summary of modENCODE Temporal Expression Profile: Temporal profile ranges from a peak of moderately high expression to a trough of extremely low expression. Peak expression observed within 06-18 hour embryonic stages, at stages throughout the pupal period.
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cDNA Clones ( 33 )
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.
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.
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.
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.
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.
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.
Liu et al., 2012, Mol. Cell. Biol. 32(24): 4933--4945
Functional analysis of the NHR2 domain indicates that oligomerization of Neuralized regulates ubiquitination and endocytosis of Delta during Notch signaling. [FBrf0220817]
Sagner et al., 2012, Curr. Biol. 22(14): 1296--1301
Establishment of Global Patterns of Planar Polarity during Growth of the Drosophila Wing Epithelium. [FBrf0219045]
Xie et al., 2012, Dev. Biol. 363(2): 399--412
Drosophila Epsin's role in Notch ligand cells requires three Epsin protein functions: The lipid binding function of the ENTH domain, a single Ubiquitin interaction motif, and a subset of the C-terminal protein binding modules. [FBrf0217494]
Xie et al., 2012, PLoS ONE 7(4): e36362
Uif, a Large Transmembrane Protein with EGF-Like Repeats, Can Antagonize Notch Signaling in Drosophila. [FBrf0218242]
Yamamoto et al., 2012, Science 338(6111): 1229--1232
A Mutation in EGF Repeat-8 of Notch Discriminates Between Serrate/Jagged and Delta Family Ligands. [FBrf0220110]
Zacharioudaki et al., 2012, Development 139(7): 1258--1269
bHLH-O proteins are crucial for Drosophila neuroblast self-renewal and mediate Notch-induced overproliferation. [FBrf0217605]
Benhra et al., 2011, Curr. Biol. 21(1): 87--95
AP-1 Controls the Trafficking of Notch and Sanpodo toward E-Cadherin Junctions in Sensory Organ Precursors. [FBrf0212697]
Cherbas et al., 2011, Genome Res. 21(2): 301--314
The transcriptional diversity of 25 Drosophila cell lines. [FBrf0213077]
Dalton et al., 2011, Cell Death Differ. 18(7): 1150--1160
Drosophila Ndfip is a novel regulator of Notch signaling. [FBrf0214123]
Grigorian et al., 2011, Dev. Biol. 353(1): 105--118
The convergence of Notch and MAPK signaling specifies the blood progenitor fate in the Drosophila mesoderm. [FBrf0213410]
Hori et al., 2011, J. Cell Biol. 195(6): 1005--1015
Synergy between the ESCRT-III complex and Deltex defines a ligand-independent Notch signal. [FBrf0216916]
Leonardi et al., 2011, Development 138(16): 3569--3578
Multiple O-glucosylation sites on Notch function as a buffer against temperature-dependent loss of signaling. [FBrf0214548]
Marcu et al., 2011, PLoS ONE 6(1): e15361
Innate Immune Responses of Drosophila melanogaster Are Altered by Spaceflight. [FBrf0212851]
Mukherjee et al., 2011, Science 332(6034): 1210--1213
Interaction between Notch and Hif-alpha in development and survival of Drosophila blood cells. [FBrf0214249]
Nicholson et al., 2011, Development 138(2): 251--260
Notch-dependent expression of the archipelago ubiquitin ligase subunit in the Drosophila eye. [FBrf0212669]
Okegbe and DiNardo, 2011, Development 138(7): 1259--1267
The endoderm specifies the mesodermal niche for the germline in Drosophila via Delta-Notch signaling. [FBrf0213233]
Park et al., 2011, PLoS Genet. 7(8): e1002241
Specification of Drosophila corpora cardiaca neuroendocrine cells from mesoderm is regulated by Notch signaling. [FBrf0215231]
Poulton et al., 2011, Development 138(9): 1737--1745
The microRNA pathway regulates the temporal pattern of Notch signaling in Drosophila follicle cells. [FBrf0213494]
Quijano et al., 2011, Genetics 189(3): 809--824
Wg Signaling via Zw3 and Mad Restricts Self-Renewal of Sensory Organ Precursor Cells in Drosophila. [FBrf0216675]
Richter et al., 2011, Nat. Cell Biol. 13(9): 1029--1039
The tumour suppressor L(3)mbt inhibits neuroepithelial proliferation and acts on insulator elements. [FBrf0215050]
Tsubota et al., 2011, Fly 5(4): 275--284
Interactions between enhancer of rudimentary and Notch and deltex reveal a regulatory function of enhancer of rudimentary in the Notch signaling pathway in Drosophila melanogaster. [FBrf0217950]
Vallejo et al., 2011, EMBO J. 30(4): 756--769
Targeting Notch signalling by the conserved miR-8/200 microRNA family in development and cancer cells. [FBrf0213063]