Worm Breeder's Gazette 11(2): 107

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.

lin-39 Mutants are Supervuls

Scott Clark and Bob Horvitz

Figure 1

Mutations that prevent the formation of competent Pn.p cells or the 
expression of vulval lineages confer a vulvaless (Vul) phenotype.  
Previously (WBG 10(2): 45 1988; WBG 10(3): 134 1988), we described the 
isolation of Vul mutations as suppressors of lin-15 multivulva 
mutations.  In a screen of 76,000 haploid genomes, we have isolated 
156 mutations that suppress lin-15(n765ts), of which 80 are Vul.  
These include mutations in unc-83, let-23, 
let-341, lin-10, 
nSix allelic lin-15 suppressor mutations (
n1490, n1760, n1872ts, n1880, n2010, and n2110 III) cause P(3-8).p to 
join the hypodermal syncytium without dividing.  This Vul phenotype is 
similar to that caused by n300, a mutation associated with the 
translocation nT1(IV,V).  In N2, the vulval equivalence group cells P(
3-8).p divide at least once and can express vulval-specific cell 
lineages, while the non-vulval equivalence group cells, P(1,2,9-11).p, 
join the syncytium without dividing.  Unlike most Vul mutants, in 
which one Pn.p cell division occurs, these new mutants appear to lack 
the vulval equivalence group.  We refer to these mutations as Supervul 
mutations to distinguish them from other kinds of Vul mutations that 
allow Pn.p cells to join the vulval equivalence group but not to 
express vulval lineages.
Chris Li (personal communication) observed that n1760 animals lack 
the anti-FMRFamide staining normally displayed by the six P(3-8).a-
derived VC neurons of the ventral cord.  In addition, ced-1; n1760 
animals possess extra cell corpses in the ventral cord.  Together, 
these observations suggest that the FMRFamide-staining VC neurons die 
in n1760 animals.  VC neuron death and vulval abnormalities were 
observed in lin-39(n709) animals by Hilary Ellis.  n709 fails to 
complement n1490 for at least the Vul phenotype, indicating that these 
six lin-15 suppressors are new alleles of lin-39.  lin-39 maps between 
sma-3 and unc-36 on LGIII.
Three of the new lin-39 mutants (n1760, n1880, n2010) are 100% Vul 
and slightly Unc, whereas n1490 and n2110 are less than 100% penetrant 
for the Vul and Unc phenotypes.  n1872ts is 100% Vul and Unc at 25 C 
and 80% Vul and Unc at 15 C.  n709 is only partially egg-laying 
defective and not Unc; however n7091nDf16 and n7091n1490 animals are 
Vul.  Surviving VC neurons are often seen in n709 animals, but Chris 
has not seen any FMRFamide-staining VC cells in n1760 animals.  These 
data indicate that n709 is probably a weak allele of lin-39.That both 
the Pn.a and Pn.p lineages are abnormal suggests that P(3-8) could be 
expressing a P(1,2,9,10) type of cell lineage in lin-39 animals (see 
figure below).  We are currently investigating further the nature of 
the P(3-8) cell lineages and the cause of the Unc phenotype in lin-39 
animals.
[See Figure 1]

Figure 1