Worm Breeder's Gazette 10(3): 134
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
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.