Two alleles of
sel-5 were initially identified as suppressors of the egg-laying defect of the gain of function
lin-12(
n302) mutation (Tax et al., 1997). In the same study
sel-5 was also shown to function, by mosaic analysis, in the presumptive VU cell (same as
lin-12 ). We have extended that analysis with several
lin-12 mutants and show that the suppression by
sel-5 is dependent on the severity of the
lin-12 mutation. We also show that
sel-5 is unable to suppress the activated
lin-12(intra) allele, suggesting that
sel-5 functions upstream of the activating cleavage event. Consistent with this,
sel-5 does not seem to affect the transcriptional feedback regulation in Z1.ppp and Z4.aaa that establishes one as a signaling cell and the other as receiving. We also do not see an effect of
sel-5 on
lin-12 in other tissues where the latter is known to function. We have cloned
sel-5 and shown that it encodes two forms of a protein that share an amino-terminus with homology to ser/thr kinase catalytic domains. Initial subcellular localization experiments suggest that the proteins are cytoplasmic. Furthermore, both forms are able to rescue
sel-5 mutants. During the genetic analysis of
sel-5 , we discovered that while mutants in this gene do not interact with
lin-12 in the vulval precursor cells (VPCs), these mutants did partially suppress the vulvaless phenotype of some primary pathway mutants. So far, we have only seen suppression of
let-23(
sy1) ,
lin-2(
e1309) and
lin-7(
e1413) , but not of
let-23(
n1045) ,
sem-5(
n2019) , or
lin-10(
n1390) . We will present data on the localization of LET-23 in these mutants and will speculate on what this all means.