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.

Is it lin or is it let?

Scott Clark and Bob Horvitz

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