Our attention has focused on identifying targets of Ras/MAP kinase signaling that control vulval morphogenesis. To facilitate identification of morphogenesis genes, we designed a screen to recover genes that may have dual roles in vulval morphogenesis and earlier essential morphogenesis processes. Since a null mutation in such a gene might be lethal, we instead screened for rare, TS mutations. Egl- mutants, both TS and non-TS alleles, with visible defects in vulval morphogenesis but normal lineages were further analyzed as were TS alleles with lineage defects. We have screened approximately 23,000, EMS-treated, F1 chromosome sets and have isolated more than 50 mutations with a variety of intriguing phenotypes. Genetic analysis of many such mutations is in progress. Six mutations, that define four morphogenesis genes, have defects in establishing a connection of the vulva to the uterus (not connected or noc mutants) and have been further examined. The
noc-1 gene, on the X chromosome, is defined by two alleles,
ku194 and
ku205. In
noc-1 mutants, the anchor cell fails to penetrate between the vulF cells and appears to remain unfused with the uterine seam cell (utse), allowing no channel to form between the uterus and the vulva. We have obtained plasmid rescue of
noc-1(
ku194).
ku207 and
ku209 define
noc-2 and map to the X chromosome.
ku207 and
ku209 have a phenotype similar to that of
noc-1 mutants although the anchor cell occasionally has an unusual bloated appearance.
ku211 defines
noc-3 and lacks a proper uterine vulval connection because the thin utse cell process that separates the uterus from the vulva does not appear between the two organs. Instead, the tissue between the uterus and the vulva is thick and disorganized.
noc-3(
ku211) maps to chromosome II near
dpy-10.
ku212, on chromosome IV, defines
noc-4 and has a phenotype similar to that of
noc-1.