spry, Sry
membrane associated or secreted antagonist of FGF signaling - functions during tracheal development - mutant follicle-cell clones demonstrates an essential role for Sprouty in restricting Egfr activation throughout oogenesis
Please see the JBrowse view of Dmel\sty for information on other features
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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 5.50
Gene model reviewed during 5.56
3.2, 2.8, 1.7 (longest cDNA)
591 (aa); 63 (kD predicted)
sty protein is a putative secreted protein with a conserved cysteine-rich motif.
Interacts with DRK and RasGAP1 proteins of the Ras pathway.
The Cys-rich domain is responsible for the localization of the protein to the plasma membrane.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\sty using the Feature Mapper tool.
Comment: reference states 5-22 hr AEL
Comment: notum
GBrowse - Visual display of RNA-Seq signals
View Dmel\sty in GBrowse 23-8
3-6.9
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: sty CG1921
sty acts as an antagonist of EGF as well as FGF signalling pathways.
Loss of sty in the eye imaginal discs results in transformations of cone cell to R7 and mystery cells to outer photoreceptors. Loss of sty in the embryonic chordotonal organ precursors and embryonic midline glia results in supernumerary neurons, or supernumerary glia, respectively. Overexpression results in phenotypes that resemble loss of function Egfr phenotypes.
sty acts nonautonomously in the tracheal tip cells to inhibit induction of nearby stalk cells.
sty mutations cause ectopic branches to form on the stalks of primary branches in the tracheal system.
In sty mutants twice the wild type number of terminal branches form. These arise from a doubling in the number of terminal cells, these extra terminal cells arise from a fate transformation of neighbouring tracheal cells.