Gap1, mip, Gap, GTPase-activating protein 1, sextra
Ras GTPase-activating protein with PH domain and C2-domain - functions in cone cell precursors to down-regulate Ras1
Please see the JBrowse view of Dmel\RasGAP1 for information on other features
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Gene model reviewed during 5.44
Stop-codon suppression (UAG) postulated; FBrf0216884.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
5.5 (longest cDNA)
The group(s) of polypeptides indicated below share identical sequence to each other.
1165 (aa); 132 (kD predicted)
Interacts with sty.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\RasGAP1 using the Feature Mapper tool.
Enhancer trap expression is observed in third instar larvae in the eye imaginal disc posterior to the morphogenetic furrow. It is observed in all photoreceptor and cone cell precursors as well as in still uncommitted cells. Expression is also observed in a subset of cells in the antennal, wing, and leg discs and in the larval CNS.
GBrowse - Visual display of RNA-Seq signals
View Dmel\RasGAP1 in GBrowse 23-31
3-31
3-24.2
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: Gap1 CG6721
Source for identity of: RasGAP1 Gap1
FlyBase curator comment: Renamed from 'Gap1' to 'RasGAP1' because: i) 'RasGAP1' is more specific and informative; ii) 'RasGAP1' (or similar derivatives) has been used to refer to this gene in the literature.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Shows no genetic interaction with sdk.
Germline clonal analysis shows that Gap1 is required in the somatic follicle cells and not the germ line for embryonic dorsoventral polarity determination.
Mutations of Gap1 are capable of suppressing sev and boss amorphic mutations and of triggering normal R7 development. Gap1 functions downstream of boss and sev in determining the R7 cell fate. Mosaic analysis demonstrates that Gap1 mutations act autonomously in the presumptive cone cells to cause their development as supernumerary R7-like cells.
Gap1 function is cell autonomous, wild type function is required only in the cells that have the potential to become R7 photoreceptor cells.
Mutations in Gap1 cause hyperinnervation of the retinotopic map without altering is basic configuration. The extra nerve terminals in the medulla have originated from proliferation of inner photoreceptors in the developing eye.
