Caenorhabditis elegans


CELE_F13B9.5, sur-3, sar-2, F13B9.5
ksr-1 encodes one of two C. elegans Kinase Suppressor of Ras paralogs; during development, ksr-1 functions singly to control sex myoblast migration and redundantly with ksr-2 to control development of the vulva, excretory system, and male spicules; as ksr-2; ksr-1 doubly mutant animals have severely reduced or absent MPK-1/ERK diphosphorylation levels in somatic tissue, KSR-2 and KSR-1 likely function to positively regulate signaling through the LET-60/Ras pathway; genetic analyses have identified a number of ekl (enhancer of ksr-1 lethality ) mutations that, in combination with a ksr-1 null mutation, result in defects in excretory duct cell fate specification accompanied by larval lethality; the ekl mutations identified gene products that are maternally required for duct cell fate specification and encode proteins likely to be involved in transcriptional and post-transcriptional gene regulation.
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  • Interactors 11
  • Interactions 13
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