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.

age-1 is allelic with daf-23

Takao Inoue, Elizabeth A. Malone, James H. Thomas

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 27 but not at the standard assay condition of 25
(M. Ailion and J. H. T., pers. comm.), age-1 strains were tested at both
25 and 27. At 27, TJ1052 age-1(hx546) formed 100% dauers. (This
phenotype is sensitive to very small fluctuations in the temperature.
Differences as small as 0.5 may cause significant changes in the
frequency of dauer formation.) Two other age-1 strains (TJ412 and TJ401)
also formed many dauers at 27. At 25, 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 27,
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.