High impact information on ksr-1

• Our genetic analysis showed ksr-1 positively mediates Ras signaling and functions downstream of or in parallel to let-60 [1].
• Genetic epistasis analysis suggests that ksr-1 acts downstream of or in parallel to let-60 ras [2].
• By screening for mutations that suppress the vulval defects caused by a constitutively active let-60 ras gene, we identified six loss-of-function alleles of ksr-1, a novel C. elegans gene [1].
• The C. elegans ksr-1 gene encodes a novel Raf-related kinase involved in Ras-mediated signal transduction [2].
• Double mutant analysis suggests that sur-6 PP2A-B acts downstream or in parallel to ras, but likely upstream of raf, and functions with ksr-1 in a common pathway to positively regulate Ras signaling [3].

Biological context of ksr-1

• By screening for suppressors of the Multivulva phenotype caused by an activated let-60 ras allele, we isolated mutations in a gene, ksr-1, that acts as a positive modifier of vulval induction and is required for at least two other let-60 ras-mediated processes [2].
• C. elegans ksr-1 and ksr-2 have both unique and redundant functions and are required for MPK-1 ERK phosphorylation [4].

Anatomical context of ksr-1

• In C. elegans, ksr-1 is only required for a specific Ras-mediated process (sex myoblast migration) and is a nonessential positive regulator of other Ras-mediated developmental events [4].
• We report the existence of a second C. elegans ksr gene, ksr-2, which is required for Ras-mediated signaling during germline meiotic progression and functions redundantly with ksr-1 during development of the excretory system, hermaphrodite vulva, and male spicules [4].

References