We have isolated three new EMS-induced alleles of
age-1 (
z10,
z12, and
z25) with life spans ranging from 18.9 - 25.9 days at 25C with an average 46% increase in life span. All of these alleles fail to complement
age-1 (
hx546) for life-span extension. After backcrossing, alleles in a wild- type background were examined for resistance to several environmental stresses: heat (35C), ultraviolet light (20 J/m2) and hydrogen peroxide (0.5 M). Two replicates for the test of thermotolerance were completed on each strain. Their mean survivals (+/- SD) were 842 +/- 50 minutes (
hx546), 810 +/- 56 minutes (
z10), 862 +/- 69 minutes (
z12), and 860 +/- 81 minutes (
z25) for the
age-1 alleles compared to 562 +/- 66 minutes for wild type. All of the
age-1 alleles were significantly different from wild type (p <.001). Two replicates for UV resistance were also completed with mean survivals of 4.7 +/- 0.2 days, 4.9 +/- 0.3 days, 4.5 +/- 0.3 days, and 4.4 +/- 0.2 days, respectively. These means were compared to 3.8 +/- 0.2 days for wild type. Although the difference was significant, it was not as large as the difference for thermotolerance. One test of hydrogen peroxide resistance has shown that
z12 and N2 had a mean survival of 1.7 +/- 0.5 days while the other
age-1 alleles had mean survival of 2.6 +/- 0.2 days (
hx546), 2.6 +/- 0.2 days (
z10), and 2.7 +/- 0.6 days (
z25). This is the only environmental stress that differentiates among the
age-1 alleles.
age-1 is a constitutive dauer at 27C (Takao Inoue and Jim Thomas, this news letter). We have examined our new alleles for the Daf-c phenotype at 27C and found that after 48 hours
z10 had 90 % dauers,
z12 had 100% dauers and
z25 had 60 % dauers. We have completed this experiment three times with similar results (our
age-1 (
hx546) control has never reached 100% dauers). These alleles also fail to complement
daf-23 for the 27C Daf phenotype, as reported by Inoue and Thomas elsewhere in this volume. This is consistent with
daf-23 being allelic with
age-1, but we haven't ruled out unusual intergenic interactions being responsible for the 27C Daf phenotype.