l(2)br24, l(2)34Ea, dSos, E(sev)2A, l(2)br25
a dual specificity GEF that regulates both Ras and Rho family GTPases - integrates signals that affect gene expression and cytoskeletal reorganization - Slit-dependent endocytic trafficking of the Robo receptor is required for Son of Sevenless recruitment and midline axon repulsion
Gene model reviewed during 5.45
Gene model reviewed during 6.02
There is only one protein coding transcript and one polypeptide associated with this gene
May form a complex with sevenless and DRK.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Sos using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Sos 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.
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 cells: change from round to spindle-shaped, with the formation of F-actin puncta and microtubule extensions. S2R+ cells are unaffected.
6 alleles of Sos been recovered in a screen for mutations with mutant phenotypes in clones in the wing.
The Sos signaling pathway is required to prevent certain axons crossing the midline during the development of the central nervous system.
Identification: One of a collection of genes identified with defective larval growth that extend larval life. Not studied further due to apparent lack of association of mutant phenotype with insertion of P-element present in the mutant chromosome.
In vivo structure-function analysis revealed that the amino terminus of the Sos product is essential for its function. Membrane localization of Sos protein is independent of drk function. A drk-independent interaction between Sos and sev has been proposed that is likely mediated by the pleckstrin homology domain within the amino terminus of Sos.
The role of the N and C terminal regions of Sos are studied in mammalian cells to directly measure the effect on p21ras loading with GTP. Results demonstrate a functional role for pleckstrin and Dbl domains within the Sos protein.
A high affinity binding site for the drk SH3 domain maps to the Sos product tail. The N-terminal drk SH3 domain is primarily responsible for binding to the tail of the Sos product in vitro, and for signalling to the Ras85D product in vivo.
Experiments on Ras activation in signal transduction by human insulin receptor in COS cells found heterologously expressed Sos gene product in a complex with insulin receptor and GRB2 or p85.
In vitro, drk binds the C terminal tail of the Sos product through the drk SH3 domain, thereby linking receptor tyrosine kinases to Ras activation.
The Sos gene product is common to the sev as well as the Egfr receptor tyrosine kinase pathway but the interaction of Sos with Egfr is limited to the developing eye. Suppression of sev by Sos is allele specific.
Sos is required for photoreceptor development, acts in R7 and is a suppressor of the Egfr phenotype to restore the eye to a nearly normal appearance.
Recessive lethal or semi-lethal; heteroallelic or hemizygous escapers have small rough eyes; heterozygotes between two weak alleles viable with rough eyes.