Worm Breeder's Gazette 10(2): 45

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.

Of Supermuvs and Supervuls

Scott Clark and Bob Horvitz

Mutations that alter the vulval cell lineages have been previously 
identified by screening directly for animals that either lack a 
functional vulva (Vulvaless) or possess ectopic vulvae (Multivulva).  
The analysis of these mutations and laser ablation experiments has 
suggested a model for the development of the vulva.  To define further 
the genetic pathway of vulval development, we are isolating extragenic 
suppressors and enhancers of lin-15 mutations.  Mutations in lin-15 
perturb the determination of vulval cell fates and confer a multivulva 
(Muv) phenotype.
The F2 progeny of EMS-mutagenized lin-15(n765ts) animals were 
screened at the restrictive temperature (22.5 C) for animals that 
either lacked or possessed additional ventral protrusions.  Four 
allelic mutations (n1614, n1615, n1616, n1730 I) were found that 
increase the number of protrusions present on lin-15 animals.  n1614 
also enhanced the phenotype of other Multivulva mutants, lin-1(e1777), 
1); 2) and lin-12(n137); that is,
n1614 converted the Muv phenotype of these mutants into a Supermuv 
phenotype.  Alone, these new mutations cause the preanal region to be 
slightly swollen in hermaphrodites.  Limited lineage analysis of 
strains carrying only these enhancing mutations indicates that in 
hermaphrodites P9.p can divide and adopt a 3  cell fate.  (In N2 
hermaphrodites, only cells in the vulval equivalence group, P(3-8).p, 
divide while the other non-vulval equivalence group Pn.p cells join 
the syncytium without dividing.)  These observations suggest that P9.p 
may be transformed in this mutant from a non-vulval equivalence group 
cell to a vulval equivalence group cell and consequently be affected 
by vulval-specific lineage mutations.
Mutations that prevent the generation of competent vulval precursor 
cells are known to be epistatic to lin-15 mutations and to yield a 
vulvaless (Vul) phenotype.  In our screen, we have isolated three 
alleles of unc-84(n1534, n1612, n1756) and two alleles of a novel gene 
(n1490, n1760 III) of this class.  unc-84 mutations block the 
migrations of the P cells and cause the animals to be both vulvaless 
and uncoordinated.  The mutations n1490 and n1760 prevent the division 
of the Pn.p cells, a phenotype similar to that caused by the mutation 
n300, which is associated with the translocation nT1(IV,V).  However, 
because they are slightly uncoordinated, n1490 and n1760 mutants 
probably have other lineage defects .  n1490 is also epistatic to lin-
1(e1777) and to lin-15(n309).   In addition, n1614; n1490 and n1614; 
n1490; lin-15(n765) animals are vulvaless.  One possible explanation 
for the mutant phenotype of n300, n1490 and n1760 animals is that 
vulval equivalence group cells are transformed to non-vulval 
equivalence group cells.  Such mutations, which eliminate the vulval 
equivalence group, can be regarded as Supervul mutations.