R, Roughened, Dras3, Rap, l(3)62Bf
Ras-like GTPase - establishes of cell polarity by regulation of columnar cell shape - controls epithelial invagination via α-Catenin - regulates cell morphology within the developing wing epithelium - regulates radial movement of mesodermal cells during monolayer formation - regulates adhesive contacts necessary for maintenance of Egfr signaling between cells and differentiation of wing veins and photoreceptors
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.45
2.9, 1.9, 1.5 (northern blot)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Rap1 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Rap1 in GBrowse 2
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 merge of: R BEST:GH18528
Renamed from 'R' to 'Rap1' to represent community usage and to minimise confusion with the 'r' ('rudimentary') gene symbol, from which it differed only by case.
R and cno proteins act in the same molecular pathway during dorsal closure and the function of both proteins in dorsal closure depends on their ability to interact with each other. R acts upstream of cno in dorsal closure, but unlike cno, is not involved in the stimulation of JNK pathway activity.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a phenotype when assayed in Kc167 and S2R+ cells: cells become round and detached.
Cells mutant for R condense their adherens junctions to one side of the cell in clones in the wing. This disrupts normal epithelial cell behaviour, leading to the mutant cell clones dispersing into the surrounding wild-type tissue.
Ras85D-mediated signalling pathways are not influenced by R levels. Ras85D and R seem to function via distinct pathways. R has a regulatory role in morphogenesis in the eye, ovary and embryo. R also plays a role cell migration and cell shaping.
Candidate gene for quantitative trait locus.
Analysis of genetic interactions among faf and R and Ras85D reveals that in addition to its critical role anterior to the morphogenetic furrow, faf has a function in undifferentiated cells alter in eye development that involves, probably indirectly, Ras85D and R. These results suggest that cells outside the facet influence cell fates within the facet.
R is essential for cell proliferation although it is not required for cell survival in post-mitotic cells. It is also required during oogenesis.
R mutations disrupt the normal cell fate specification in photoreceptor cells.
The transcription pattern of R was analyzed in neuroblasts derived from tumorous larval brain of l(2)gl larvae and S2 tissue culture cells. R expresses constitutive as well as maternal/embryonic-specific transcripts.
An unusually low recovery rate of certain classes of deletions for the R locus suggests that a chromosome interval within 62B3-4 to 62D3-4 may be dominantly sensitive to position effects.
Isolated as a Ras homologue, but also found to share high homology with human Rap.