Worm Breeder's Gazette 10(3): 132

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.

Suppressors of lin-15 Multivulva Phenotype Define New Genes Involved in the C. elegans Vulval Induction

Raffi Aroian, Min Han, Ron Rogge and Paul Sternberg

The vulva of C.  elegans is generated when three of six vulval 
precursor cells (VPCs) are induced to divide and form vulval cells.  
Mutations in the multivulva (Muv) class of genes result in more than 
three VPCs forming vulval cells; mutations in the vulvaless (Vul) 
class of genes result in fewer than three VPCs forming vulval cells (
often causing an egg-laying defect).  Mutants which carry both a Muv 
and a Vul mutation can display either phenotype, depending on the 
particular pair of mutations present.  In some cases, Muv and Vul 
mutations are mutually antagonistic.  For example, most animals 
carrying both lin-16(n309), a strong Muv mutation, and let-23(sy1), a 
strong Vul mutation, are Vul, but some worms have one or several 
ventral protrusions normally associated with the Muv phenotype.  In 
addition, the egg-laying defect is less severe in the double mutant 
than in the Vul mutant alone.  Understanding the basis for this 
antagonism is important for modelling the pathways involved in vulval 
induction.  To further establish the relationship between Muv and Vul 
genes and to isolate new alleles and genes that participate in vulval 
induction, we have isolated extragenic suppressors of a Muv mutation.
Multivulva lin-15(n309) worms were mutagenized with EMS, and the F2 
were screened for non-Muv progeny.  To date, 50,000 F1 chromosome sets 
have been screened, and ten independent mutations have been isolated.  
Two of these, sy1 and sy97, are recessive, Vul let-23 alleles; two 
others, sy93 and sy96 IV, are also recessive and are Vul in 
combination with lin-15(n309).  The mutations sy1, sy96, and sy97 are 
Vul in a lin-15(+) background, and the penetrance of the syl and sy97 
Vul phenotypes are somewhat suppressed by lin-15(n309).  We have also 
identified a class of suppressors, sy95 and sy100, that suppress the 
Muv phenotype of lin-15(n309) and are Vul in a lin-15(+) background, 
but appear wild-type if combined with lin-15(n309).  That is, the Vul 
phenotype and lin-15(n309) Muv are mutually suppressed.
Six of our ten isolates (sy92, sy94, sy95, sy99, sy100, sy101) 
harbor dominant Vul mutations, and thus define a new class of 
mutations affecting vulval induction.  All but sy95 and sy100 are 
epistatic to lin-15(n309) (see above).  Two of these mutations, sy99 
and sy101, have been mapped to LGIV.  Both mutations are recessive 
larval lethals; at least one has a dominant male-defective phenotype.  
These mutations appear to be distinct from the previously identified 
dominant generation Vul mutations lin-24 and lin-33 (also on LGIV) in 
that lin-24 and lin-33, unlike our mutations, cause the death of VPCs (
Ferguson et al., Nature 326, 259, 1987).  Since dominant mutations in 
the vulval developmental pathway that do not result in VPC generation 
defects are uncommon (lin-12 and lin-34 are the only other ones), we 
are intrigued as to what new information will come from analysis of 
these dominant Vul mutations.