Both
age-1 and
daf-23 mutants show a life-extension (Age) phenotype under some conditions.
age-1 mutants form dauer only at semi-lethal 27 oC, whereas
daf-23 mutants are non-conditional dauer formers with a strong maternal effect. Recently, Malone et al., 1996 and Morris et al, 1996 observed that
age-1(
hx546) fails to complement
daf-23 alleles for Daf-c and Age phenotype. They concluded that
age-1 and
daf-23 are allelic. The latter also found mutation sites in a PI3 kinase gene in
daf-23 alleles but not in
age-1(
hx546). We have sought the location of
age-1 mutation sites, because such information could provide an insight into the !healthy! life extension of
age-1 mutants and an absebce of the maternal effect. Direct sequencing has been used to determine the mutation sites in four
age-1 alleles,
hx546,
z10,
z12, and
z25. We have completed sequencing the PI3 kinase gene including the introns in
hx546 and
z25 and almost completed
z10 and
z12; no mutation site has been found. This argues against the conclusion that
age-1 and
daf-23 are the same gene. Thus, we have re-tested the genetic complementation. Though we have obtained similar results to the previous work, we found two separable Daf-c Age mutants in the
age-1(
hx546) strain (we provisionally call them
age-1(L) and
age-1(R); see also 1996 West Coast Meeting Abstract 137). Both fail to complement
daf-23 mutations. This implicates non-allelic non-complementation between
age-1(L),
age-1(R) and
daf-23. Since only the complementation data suggest
age-1/daf-23 allelism, it is not clear that
age-1 and
daf-23 are the same gene.