To define further the genetic pathway of vulval development, we have been isolating extragenic suppressors of
lin-15 mutations.
lin-15 mutations perturb the determination of vulval cell fates and cause a multivulva phenotype. In addition to the suppressor mutations described previously (WBG 10(2): 45 1988), we have identified several mutations that variably confer a vulvaless phenotype and a distinctive rod-like larval lethal phenotype. These phenotypes are reminiscent of phenotypes caused by mutations in
let-23, an essential gene known to function in the determination of vulval cell fates. One mutation of this class,
n1613 V, is temperature-sensitive for the larval lethality, the vulvaless phenotype, and the suppression of
lin-15(
n309). This mutation was found to be allelic with an essential gene identified by David Baillie's laboratory,
let-341(
s1031,
s1415,
s1421,
s2118). The terminal arrest phenotype of
s1031 animals appears similar to that exhibited by
n1613,
n1613/Df or
n1613/s1031 animals at 25 C. Another incompletely penetrant lethal allele of
let-341,
n1822, has additionally been found as a suppressor of
lin-15. Animals carrying another mutation,
n1619 X, most often die as larvae, and those that survive are vulvaless. Lineage analyses of
n1613 and
n1619 strains reveal that all six vulval precursor cells tend to adopt 3 cell fates. These two mutants also display a partially penetrant weak multivulva phenotype like that seen in
let-23 mutants. Mutations in
lin-1, which cause a multivulva phenotype, can suppress the lethality associated with
let-23 mutations.
lin-1 mutations can similarly suppress the lethality caused by both
n1613 and
n1619. We believe it likely that
let-23,
n1619) function together in the determination of cell fates because of the many shared properties of these genes. We have screened for mutations that suppress the lethality of let- 341
(n1613ts). As expected, we have isolated additional alleles of lin- 1
(n1814,
n1815,
n1816,
n1817,
n1848). We have also identified a mutation,
n1849 IV, that is a partially dominant suppressor of the lethality of
let-341(
n1613ts) and confers a semidominant multi vulva phenotype. The map position and Muv phenotype of
n1849 suggest that it may be an allele of
lin-34 (see article by Greg Beitel and Bob Horvitz this gazette). We next determined whether the canonical allele of
lin-34,
n1046, could suppress the lethality of the
n1619 mutation or of putative null alleles of
let-23 and
let-341. Like
n1849,
n1046 is a partially dominant suppressor of the lethality associated with
n1619,
let-341(
s1031) and
let-23(
mn23,
mn216,
mn224). Interestingly, the multivulva phenotype of
lin-34(
n1046) is significantly suppressed by the lethal mutations
n1619 and
s1031. This reciprocal suppression is difficult to evaluate for the three alleles of
let-23 because
let-23; are sterile (unlike
lin-34;
n1619 or
lin-34; 1031) doubles, which are fertile). The nature of the interactions among these genes reinforces the notion that at least four genes,
let-23, 9), and
lin-34, are collectively involved in a decision-making process that occurs in both vulval and nonvulval cells.