lin- 12
(n676n930) is a temperature sensitive hypomorphic allele. Homozygous hermaphrodites grown at 25 C are Egl and display incompletely penetrant,
lin12(0)-1ike defects in the AC/VU decision, VPC fate determination, and germline development. In addition, temperature shift experiments have revealed an unknown 'late defect', which might involve HSN function. We reverted the Egl phenotype of
lin-12(676n930) and obtained 26 EMS- induced extragenic suppressors at a total frequency of 5 X 10-5. Coordinate suppression of all or most of the original
lin-12(676n930) defects is seen in revertant animals. We have named the suppressor loci 'sel' genes, for 'suppressor/enhancer of
lin-12', since we have found that some of these mutations can enhance gain of function
lin12(d) alleles in addition to suppressing
lin12(676n930). Thirteen dominant sel mutations, including sel
(ar40), map very close to
dpy-5 on linkage group 1. The remaining sel alleles, including
sel-1(
e1948), sel
(ar22), sel
(ar41), and sel
(ar84), are recessive and define four complementation groups all mapping between
rol-3 and
unc-42 on linkage group V. Genetic studies suggest that the sel mutations may not be simple reduction of function alleles. For the majority of sel genes, the identification of null alleles has been complicated by the fact that sel/Df neither suppresses
lin12(676n930), nor has a discernible phenotype in a
lin12(+) background. To investigate further the nature of the sel mutations, we have analyzed the phenotype of
lin12(n676n930) ; sel/sel/+ hermaphrodites. Such dosage experiments, as well as interactions between sel mutations and different
lin-12 alleles, will be described.