Worm Breeder's Gazette 13(5): 83 (February 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.

A Common Phenotype of Longer Life Mutants In C. elegans.

Shin Murakami, Thomas E. Johnson

Institute for Behavioral Genetics, University of Colorado. Campus Box 417, Boulder, C0 80309-0447, USA. e mail: murakams@ibg.colorado.edu

Longer life may come from a single mechanism in C.elegans.
It has been proposed that longer life span can be achieved
either by reduction of sperm formation (1), or by turning
on some aspects of dauer formation (2). As a first step to
understand the basis of longer life, we have searched for
phenotypes shared among all the long-life mutants: age-l,
daf-2 and spe-26. We excluded rad-8, because its life extension
is due to delayed differentiation. An environmental stress,
UV light, has been suggested as a factor that accelerates
aging. We have focused on resistance to UV irradiation
as a candidate phenotype.
All the longer-life mutants showed more resistance to
UV irradiation than wild type, N2. First, we tested whether
age-l mutants were more resistant to UV at various energies
from 5 to 60 J / m2. Immediate death of the hermaphrodites
was observed at energies of more than 60 J / m2 so we have not
examined higher doses than this. At energies from 5 to 40
J / m2, age-l mutant showed significantlygreater survival
after the irradiation than wild type in 12 independent
experiments. It is unlikely that this results from self-imposed
dietary restriction (eating less or more extends life),
because we could not find any difference in the percentage
of worms pumping or in the pumping rate after UV. age-l survival
after UV irradiation is also significantly different
from wild type at 20 J / m (P < 0.0001; wild type: 3.2 -4.4 days;
age-l: 4.6 - 5.9 days). However, the percentage of immediate
death after the UV irradiation was similar between age-l
and wild type, which is consistent with a previous study
(3). This suggests that initial UV damage was similar between
age-l and wild type. The recovery from the damage can be
more efficient in age-l than in wild type. Similar results
were obtained using daf-2 (el370), spe-26 (hc138) and
spe-26 (it118) at 20 J / m2. In addition, there appeared
a correlation between mean life span and the level of UV
resistance (Fig. I; mean life span data used in the figure
is from Ref.l, 2 and our results).
Increased UV resistance was the first common phenotype
seen in all of the longer-life mutants. Recently, similar
results were obtained by checking increased thermotolerance
(see Lithgow et al., in this issue). We would like to propose
that a single mechanism which confers stress resistance
also causes a longer life span in C elegans.
1 Van Voorhies. 1992. Nature. 360: 456458. 2 Kenyon et al.,
1993. Nature. 366: 461464. 3 Hartman et al., 1988. Mutation
Research 208: 77-82.