Worm Breeder's Gazette 6(1): 40

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A Complex Locus Affecting Vulva Development in C. elegans

I. Greenwald, C. Ferguson, N. Tsung, B. Horvitz

Figure 1

We have identified several classes of mutations affecting vulva 
development in C.  elegans that map within a small region of LGIII 
near unc-32.(1) lin-9(n112), in combination with lin-8(n111) II 
confers a multivulva (Muv) phenotype.  The lin-9(n112) mutation alone 
confers no visible phenotype.
(2) lin-12(n137, n177, n427) are semidominant Muv mutations.  
Heterozygous males mate well and generally have a single protrusion 
near the tail; homozygous males are unable to mate and have several 
pseudovulvae along the ventral side.  Both heterozygous and homozygous 
hermaphrodites have multiple pseudovulvae and almost never have a 
functional vulva, although heterozygotes are distinguishably healthier 
than homozygotes.
(3) n302 is a dominant vulvaless (Vul) mutation.  Approximately 2/3 
of the heterozygous and >99% of the homozygous hermaphrodites are Vul. 
The homozygous males are able to mate and appear to have a wild-type 
phenotype.
(4) n379 is a dominant Vul mutation of incomplete penetrance.  
Approximately 1/20 of the heterozygous and 95% of the homozygous 
hermaphrodites are Vul.  The homozygous males are able to mate and 
appear to have a wild-type phenotype.
(5) At least 7 tightly linked revertants of n137 and n177 are 
recessive weak to moderate Vul at 25 C but semidominant Muv at 15 
C
(6) At least 2 tightly linked revertants of n302 are recessive weak 
Vul at 25 C but semidominant Muv at 15 C.
(7) At least 3 tightly linked revertants of n302 are weak Vul at all 
temperatures.
Revertants of n137, n177, and n302 were isolated by picking eggs 
laid by F2 progeny of hermaphrodites mutagenized with EMS.  Unlinked 
recessive and unlinked dominant suppressors of n137, n177, and n302 
were also isolated.
Not all complementation tests among these various mutations, and 
between these mutations and  have been completed.  We do 
not yet know the number of complementation groups involved, but the 
patterns appear to be complex: some of the heterozygous combinations 
have phenotypes intermediate between those of the parents, and others 
appear to have more extreme (suppressed or enhanced) phenotypes.  The 
data so far suggest that these mutations define genes that interact to 
affect vulva development.
[See Figure 1]
nDf17 was isolated by complementation screening: N2 males were 
mutagenized with gamma-rays and crossed with unc-36(e251)dpy-18(e364) 
hermaphrodites.  F1 Unc-36 progeny hermaphrodites were crossed with 
males heterozygous for LGIII markers to determine if a deficiency was 
generated.

Figure 1