unc-101 mutations confer an Unc phenotype and suppress the vulval defect of weak
let-23 alleles. We are interested in the genetics and molecular biology of this locus because of its broad range of phenotypes and interaction with
let-23.We have attempted to identify a null allele of
unc-101. We have used trimethyl-psoralen (TMP), which produces small deletions at high frequency (Edgar et al. WBG 11(2) 79) , as a mutagen in a screen for mutations that fail to complement unc- 101
(rh6). Out of 11,000 F1 cross-progeny hermaphrodites, one new allele,
sy216, was recovered. This allele is a homozygous lethal.
sy216 homozygotes arrest in the L1 stage but remain alive for 5-6 days. The lethality of other alleles can be rescued by maternal expression, but the lethality of
sy216 cannot be rescued, since no Dpy segregate from
dpy-5(
e61)
y216)/++ heterozygous hermaphrodites. Because this allele is more severe than the existing 6
unc-101 alleles, we consider this allele a putative null allele of
unc-101.
sy216 does not delete
unc-75, it overlap eDf3. We still do not know whether this mutation is a point mutation in
unc-101 or a deletion of
unc-101 and as yet unidentified flanking gene(s). We have tried to find extragenic suppressors of
unc-101. We screened the F2 progeny of 20,000 EMS mutagenized F1 chromosome sets of
unc-101(
sy108) and
dpy-5(
e61)
h6) and have not recovered any candidates. We are currently trying to clone
unc-101 using parallel RFLP mapping with the congenic strain used for cloning
ced-1 (Gerber et al. WBG 11( 4) 24) which was kindly provided by Bob Horvitz's lab. Further mapping of
unc-101 places it to the left of
let-201,
let-202,
let-203 and the left end of eDf3. Therefore
unc-101 is not a recessive hypermorph, which we had previously suggested. [See Figure 1]