CELE_C54D1.6, pvl-1, spy-1, C54D1.6

bar-1 encodes a beta-catenin; during C. elegans development, BAR-1 likely functions as a transcriptional coactivator whose activity is required for Q neuroblast migration, P12 cell fate specification, and P3.p through P8.p vulval cell fate specification at two different stages of development; in specifying vulval cell fates, bar-1 interacts with Wnt and MAPK signaling pathways to regulate proper expression of the LIN-39 homeodomain transcription factor, overexpresion of which can partially rescue the bar-1 mutant phenotype; in yeast two-hybrid assays, BAR-1 interacts strongly with the POP-1/TCF transcription factor, and when fused to the Gal4 DNA binding domain, BAR-1 can function in yeast as a transcriptional coactivator; during larval development, BAR-1 expression begins in P3.p through P8.p at the late L1 stage and then disappears from these cells by the mid-L3 stage; BAR-1 is also expressed in P12, in the seam cells, and in cells of the somatic gonad; BAR-1 subcellular localization, assessed using an integrated transgene, reveals localization to the cytoplasm, nucleus, and cell junctions; genetic mosaic analyses indicate that, in P4.p and in P12, bar-1 acts cell autonomously to specify cell fates.

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.