Worm Breeder's Gazette 11(2): 106
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In screening 75,000 F1 mutagenized haploid chromosome sets for suppressors of the vulvaless (Vul) phenotype of non-null let-23 alleles, we recovered two alleles, sy108 and sy161, which fail to complement unc-101(m1). Both of these new alleles suppress the vulval defect of let-23(sy1), a Vul non lethal allele, as do m1 and rh6, the previously identified alleles. The lethality of the subviable let-23 allele sy97 is not suppressed. Homozygotes of all four alleles segregate some dead larvae (primarily L1, but dead eggs, L2s, L3s, L4s, and young adults can be found). This lethality can be rescued by zygotic or maternal expression (no dead larvae are present among the cross progeny if sy108 hermaphrodites are mated to N2 males) in the case of sy108. We have not yet tested to determine if this is true for all alleles. Additional pleiotrophies are seen in the amphids and phasmids (Hall and Hedgecock WBG11.1), defecation cycle (J. Thomas, in press) and male spicules (H. Chamberlin, pers. comm). We are attempting to determine a null phenotype for unc-101. In a non- complementation screen of 17,000 F1 cross progeny hermaphrodites, two new alleles, sy168 and sy169, have been recovered. These alleles are similar to the other four alleles. We have mapped unc-101 to the right of let-201, 202, and 203 and to the left of unc-59. Thus, unc- 101 should be deleted by eDf3, which fails to complement the lethals and unc-59. Animals of genotype unc-101(sy108)/eDf3 are both viable and coordinated. Similarly, sDp1 should cover unc-101 and complement the phenotype in an animal of the genotype sDp1/unc-101/unc-101. However, animals of this genotype [sDp1/dpy-5 unc-101(m1)/dpy-5 1)] are uncoordinated. We have two explanations for this observation, both of which are hard to swallow: (1) either unc-101 mutations are recessive hypermorphs or (2) unc-101 is near or is itself a haplo lethal, triplo lethal locus (i.e. a locus that is viable if and only if it is diploid). We are attempting to distinguish between these two possibilities. If the existing unc-101 mutations are gain-of-function and unc/Df is wild type and viable, then null alleles should be recoverable as F1 suppressors of the Unc phenotype. To date, we have screened 18,000 EMS mutagenized F1 chromosome sets and have not recovered any candidates; we are currently screening X-ray mutagenized animals for F1 revertants. On the other hand, if unc-101 is or is near a haplo triplo lethal, then eDf3 is actually a complex deficiency and it should be possible to recover new unc-101 alleles on the eDf3 chromosome in a non- complementation screen. [See Figure 1]