Worm Breeder's Gazette 7(2): 48
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.
The mutant n695 was isolated by Chip Ferguson during a general screen for animals defective in egg-laying. This mutant is incompletely dominant and weakly temperature-sensitive. The phenotype of n695 ranges from egg-laying defective hermaphrodites (bloated with late stage eggs) to animals that have a male body shape and size and an abnormal male-like tail. Like N2 males, n695 hermaphrodites lack hermaphrodite-specific neurons (HSN'S), apparently because these animals express the normally male-specific program for HSN cell death ( See Ellis and Horvitz, this Newsletter). The n695 male-like animals described above appear to be XX in genotype. (i) If these animals were XO, n695 must be producing nullo- X gametes at a high frequency. No evidence for increased X-chromosome non-disjunction was observed when lon-2 males were crossed with dpy-11 n695 hermaphrodites and the cross progeny scored for matroclinous Lon males. (ii) The mutant dpy-21(e459) causes XX animals to be Dpy and XO animals to be non-Dpy regardless of sexual phenotype (Hodgkin, Genetics, 96, 649, 1980). In the n695 dpy-21 double, the abnormal males are Dpy, indicating that they are XX in genotype. (iii) n695 XO animals were generated by constructing a double with him-5. This strain produces wild-type (presumably XO) males as well as abnormal males. These observations indicate that n695 transforms, with variable expressivity, XX animals into abnormal males and has no obvious effect on XO animals. HSN development appears to be particularly sensitive to this transformation in sexual phenotype. n695 maps to a position close to that of her-1 V. Recessive alleles of her-1 transform XO animals into fertile hermaphrodites and have no apparent effect on XX animals (Hodgkin, ibid.). If the phenotype of recessive her-1 alleles results from the loss or reduction of her-1 gene activity, the phenotype of n695 might result from an increased or altered activity of this locus. In this case, elimination of n695 activity by reversion of the n695 phenotype should generate her-1 alleles. n695 revertants were isolated, and two of three apparently intragenic revertants failed to complement e1518, a recessive her-1 allele. This result strongly suggests that n695 and the recessive her- 1 alleles represent alternate states of the same gene. It is unlikely that her-1 is a tightly linked, extragenic suppressor of n695 because the her-1 mutation in the revertants is cis-dominant: revertant heterozygotes (n695 her-1/+) are wild-type, but n695/e1518 heterozygotes are predominantly mutant.