Worm Breeder's Gazette 14(1): 99 (October 1, 1995)
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.
Department of Genetics University of Washington Box 357360 Seattle, WA 98195-7360
Dauer-constitutive (Daf-c) mutations in the genes daf-2 and daf-23 extend life span (Age) (Kenyon et al., Nature 366: 461-464, Larsen et al., Genetics 139: 1567-1583). The Age phenotypes of daf-2 and age-1 are suppressible by a daf-16 mutation (C. Kenyon, pers. comm., Larsen et al., Genetics 139: 1567-1583). These results suggested similar underlying defects in the age-1 and these Daf-c mutants, and prompted us to look at the effect of age-1 on dauer formation. Because several mutants have been identified recently that show a Daf-c phenotype at 27š but not at the standard assay condition of 25š (M. Ailion and J. H. T., pers. comm.), age-1 strains were tested at both 25š and 27š. At 27š, TJ1052 age-1(hx546) formed 100% dauers. (This phenotype is sensitive to very small fluctuations in the temperature. Differences as small as 0.5š may cause significant changes in the frequency of dauer formation.) Two other age-1 strains (TJ412 and TJ401) also formed many dauers at 27š. At 25š, none of these strains formed any dauers. To confirm that the Daf-c phenotype was caused by a mutation in age-1, the phenotype was mapped. age-1 has been assigned to linkage group II based on its Age phenotype (Friedman and Johnson, Genetics 118:75-86). Using three-factor crosses, the Daf-c phenotype was mapped between bli-1 and rol-1 on chromosome II. Because the position of the Daf-c mutation was consistent with it being a daf-23 allele, we carried out a complementation test. daf-23(mg44)/age-1(hx546) heterozygotes formed 100% dauers at 27š, indicating non-complementation. Both mutations are recessive. We also tested two additional daf-23 alleles (provided by A. Koweek and G. Ruvkun), and both failed to complement age-1. Epistasis analysis was done with age-1 and several Daf-d mutations, and the results were similar to those found with daf-23 and daf-2. daf-3, daf-5 and osm-5 failed to suppress age-1, whereas daf-16 partially suppressed age-1. Recent results from Tom Johnson's lab indicate that several independently isolated age-1 alleles are also dauer-constitutive (S. Duhon and T. Johnson, this issue). We conclude that age-1 and daf-23 are allelic and that mutations in this gene result in both Daf-c and Age phenotypes. The gene should be referred to as age-1 in accordance with the standard nomenclature. We thank C. Kenyon, S. Duhon and T. Johnson for communicating unpublished results, and A. Koweek, H. Tissenbaum and G. Ruvkun for sending unpublished mutations.