l(2)br24, l(2)34Ea, dSos, E(sev)2A, l(2)k05224
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
Please see the JBrowse view of Dmel\Sos for information on other features
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Gene model reviewed during 5.45
Gene model reviewed during 6.02
5.5 (longest cDNA)
6.0 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
1595 (aa)
1596 (aa)
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.
Expression in stage P3 pupal leg discs is ubiquitous but is elevated in the tarsal joints.
Sos protein is widely expressed at embryonic stage 12, but has begun to be enriched in developing axons.
GBrowse - Visual display of RNA-Seq signals
View Dmel\Sos in GBrowse 22-49
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: Sos CG7793
Source for merge of: Sos E(var)189
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.
Shows no genetic interaction with sdk.
Activated mutations of Sos suppress the P{sevhs-cswCS} phenotype and inactivated mutations enhance the mutant phenotype.
Loss of function alleles of Sos are enhancers of the cswEsev1A-3EC.sev and cswEsev1A-eOP.sev phenotype.
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.
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.
Sos has been cloned and sequenced.
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.