Worm Breeder's Gazette 11(4): 74
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 fundamental mechanisms of reproduction and survival are being explored through the analysis of genetic stocks that have reduced fertility and postponed senescence. age-1(hx546) is a recessive mutant allele that results in an average 40% increase in life span at 20 C and an average 65% increase at 25 C. Mutant males also show extended life spans. Associated with the increased life span is a 75% decrease in hermaphrodite self-fertility (Friedman and Johnson, Genetics 118: 75-86, 1987). The long-lived phenotype was not separable from fer-15(b26), a temperature-sensitive locus on linkage group II causing defective spermatogenesis. It was not clear whether age-1 was a further mutation in fer-15 or just tightly linked to fer- 15. We now have three separate lines of evidence to show (1) that age- 1 and fer-15 are distinct genetic loci and (2) that the decrease in self-fertility is due to fer-15, not age-1 as had previously been assumed. Multifactor Crosses: In recombinants selected between dpy-10 and unc- 4, the decreased self-fertility cosegregates with fer-15 but long life span does not. We have therefore separated lines with (1) wild-type life span and wild-type self-fertility, (2) wild-type life span and decreased self-fertility, (3) long life span and decreased self- fertility, and (4) long life span and wild-type self-fertility. Deficiency Analysis: Using a series of deficiencies covering much of the region between dpy-10 and Unc-4, the decreased self-fertility phenotype was assigned to the same region as were fer-15 and emb-27. The long life span phenotype was not assigned to this same region, but rather to a region between let-23 and unc-4. We are mapping age-1 more precisely using a second set of deficiencies through this region. Tc1 Recombinants: A Bristol/Bergerac congenic was constructed in which the Bergerac wild-type alleles of fer-15 and age-1, together with several centiMorgans of flanking DNA containing many Tc1 elements, have been introgressed into an otherwise Bristol (N2) genetic background. Recombinants of this congenic crossed with a dpy-10 age-1 ere chosen. We then assayed their Tc1 patterns, temperature-sensitive defective spermatogenesis, self-fertility, and life span. fer-15 and decreased self-fertility cosegregated and mapped to the middle of the region containing novel Tc1 bands. Life span (age-1) mapped further to the right, closer to unc-4. These three lines of evidence provide a consistent interpretation of the relationship between fer-15 and age-1. These are two separate, closely linked genes. fer-15(b26) is responsible for both temperature- sensitive defective spermatogenesis and decreased self-fertility. age- 1(hx546) is responsible for long life span. We have identified the location of fer-15 on the physical map by deletion mapping (see Tedesco & Johnson). The location of age-1 will be identified through the mapping of Tc1 and Non-Tc1 polymorphisms in the Tc1 recombinants described above. The actual cloning of the genes will involve transformation of mutants with the wild-type alleles and sequence analysis to identify the mutational events responsible for the alteration of fertility and life span.