zw3, GSK3, GSK3β, GSK-3β, GSK-3
glycogen synthase kinase - segment polarity - a key component of the β-catenin destruction complex - functions in the Wingless signaling pathway - regulates Hedgehog ligand expression along with the N-end rule ubiquitin-protein ligase Hyperplastic discs
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.55
Gene model reviewed during 5.45
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.56
Interacts with cos.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\sgg using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\sgg 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.
Source for identity of: sgg CG2621
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
12 alleles of sgg been recovered in a screen for mutations with mutant phenotypes in clones in the wing.
Candidate gene for quantitative trait (QTL) locus determining bristle number.
sgg has a dual role in mesoderm development. It acts as an antagonist in cardiogenic wg signal transduction. It also seems to be required to promote positively the formation of the tin- and dpp-dependent "dorsal mesoderm", which is a prerequisite for cardiogenesis and visceral mesoderm formation.
sgg mutations emulate the effects of high ubiquitous wg in the midgut. sgg, dsh and arm function to transmit the wg signal in the midgut in the same way as they do in the epidermis. Results suggest the wg signal transduction pathway acts in all three germ layers, the ectoderm, mesoderm and endoderm.
Clonal analysis shows that loss of sgg causes cells to adopt fates normally characteristic of wg-expressing cells and to interact with adjacent wild-type tissue to cause pattern duplications similar to those caused by ectopic wg expression.
sgg is part of a signalling pathway that is required for functions of post-embryonic development, including specification of peripheral sense organs.
sgg is required for normal specification or maintenance of regional identity in the developing wing blade. sgg may be involved in the wg pathway. sgg acts downstream of localised ap and wg expression to specify or maintain margin identity in the wing.
The sgg locus is structurally complex, encoding multiple proteins. Mutational analysis reveals a single complementation group, lethality of which is associated with the loss of two major sgg proteins. Phenotypes of flies expressing individual sgg proteins reveal some but not complete redundancy of function. Under experimental conditions, one form of the protein can carry out all known functions.
sgg is only required in cells expressing ac and sc.
Partial maternal insufficiency of sgg does not cause embryonic lethality.
The sgg gene product displays homology to Ser-Thr protein kinases: sgg may play a role in a signal transduction pathway involved in the establishment of cell identity within each embryonic segment.
Clonal analysis has shown that ac and sc gene expression is unaltered in sgg mutants. Clusters of macrochaetae are caused by the differentiation of several bristles from each proneural cluster, sgg+ is necessary for the segregation of only one bristle mother cell within the cluster.
Larval growth protracted, ceasing in the first <up>sgg2, sgg9</up>, second sgg<up>5</up>, or third <up>sgg3 and sgg10</up> larval instar; death follows. sgg10 may survive to puparium formation. Mutant cuticle tissue survives only in tergites; lacks bristles and appears etched; some deformed mutant wing tissue also observed in sgg3. sgg3, but no other allele produces viable and fertile males in combination with Dp(1;4)wm65g (Shannon et al., 1972). sgg1 and sgg10 males exhibiting maternal-zygotic interaction with Dp(1;4)mg display deletion-mirror-image duplication homeotic transformation (eye-antenna, wing and leg discs) (Robbins, 1983). Same noted in male tissue of gynandromorphs (Kaufman), sgg9 and sgg10 (Garcia-Bellido and Robbins, 1983). More recent studies with sgg32, an amorphic allele, (Bourouis et al., 1989; Ripoll et al., 1988; Simpson et al., 1988; Simpson and Carteret, 1989) indicate that sgg is involved in the developmental choice between the epidermal pathway and that of the nervous system. In homozygous clones of sgg32 formed 48 h or more before puparium formation all trichomes are replaced by chaetae in the ratio of one chaeta to four trichomes reflecting the number of cells involved in the elaboration of each structure; chaetae formed conform to positional information and genotype; e.g., wing clones resemble dorsal or ventral costal bristles or triple or double row bristles depending on their position; clones are linear when near the margins and form clumps of chaetae when distant from the margins; adventitious veins often formed in association with wing clones. In the notum scutellar clones form macrochaetae in + but not sc genotypes and microchaetae in h but not + genotypes. Clones formed later than 48 h before puparium formation form trichomes, either more densely than normal (10-21 trichomes) or in normal density (up to 10 trichomes). sgg embryos from homozygous sgg female germ line cells exhibit delayed and disordered cellularization at blastoderm; gastrulation does not occur; no differentiation of ectoderm, mesoderm, or endoderm occurs; cell division continues and the embryo becomes filled with small round cells, most or all of which stain with neuronal-specific antibodies. sgg+ embryos from sgg female germinal tissue show nearly normal blastoderm formation and gastrulation; however they are short with complete cuticles and neural hyperplasia as seen in neurogenic mutants; a lawn of hairs is seen dorsally and ventrally most of the denticle belts are lacking. Two doses of sgg+ in such embryos lead to more nearly normal cuticular development, but with odd-numbered denticle bands appearing before even-numbered ones. sgg progeny of females that carry sgg+ in their germ lines die as defective larvae with underdeveloped central nervous systems; the degree of CNS development is positively correlated with the number of maternal doses of sgg+.