Genetic variation for stress-response hormesis in C. elegans lifespan
Rodriguez Sanchez, M. ; Snoek, L.B. ; Riksen, J.A.G. ; Bevers, R.P.J. ; Kammenga, J.E. - \ 2012
Experimental Gerontology 47 (2012)8. - ISSN 0531-5565 - p. 581 - 587.
quantitative trait loci - genotype-environment interactions - nematode caenorhabditis-elegans - long-lived mutant - drosophila-melanogaster - heat-shock - history traits - natural variation - longevity - resistance
Increased lifespan can be associated with greater resistance to many different stressors, most notably thermal stress. Such hormetic effects have also been found in C. elegans where short-term exposure to heat lengthens the lifespan. Genetic investigations have been carried out using mutation perturbations in a single genotype, the wild type Bristol N2. Yet, induced mutations do not yield insight regarding the natural genetic variation of thermal tolerance and lifespan. We investigated the genetic variation of heat-shock recovery, i.e. hormetic effects on lifespan and associated quantitative trait loci (QTL) in C. elegans. Heat-shock resulted in an 18% lifespan increase in wild type CB4856 whereas N2 did not show a lifespan elongation. Using recombinant inbred lines (RILs) derived from a cross between wild types N2 and CB4856 we found natural variation in stress-response hormesis in lifespan. Approx. 28% of the RILs displayed a hormesis effect in lifespan. We did not find any hormesis effects for total offspring. Across the RILs there was no relation between lifespan and offspring. The ability to recover from heat-shock mapped to a significant QTL on chromosome II which overlapped with a QTL for offspring under heat-shock conditions. The QTL was confirmed by introgressing relatively small CB4856 regions into chromosome II of N2. Our observations show that there is natural variation in hormetic effects on C. elegans lifespan for heat-shock and that this variation is genetically determined.
Integration of a pAL2-1 homologous mitochondrial plasmid associated with life span extension in Podospora anserina
Maas, M.F.P.M. ; Sellem, C.H. ; Rincheval, V. ; Hoekstra, R.F. ; Debets, A.J.M. ; Sainsard-Chanet, A. - \ 2007
Fungal Genetics and Biology 44 (2007)7. - ISSN 1087-1845 - p. 659 - 671.
cytochrome-c-oxidase - long-lived mutant - alternative oxidase - complex-i - neurospora-intermedia - dna rearrangements - senescence - sequence - amplification - respiration
We isolated and characterized a novel spontaneous longevity mutant of Podospora anserina strain Wa32 carrying one of the pAL2-1 homologous mitochondrial plasmids. This mutant is at least ten fold longer-lived than the wild type, and is hence a formal suppressor of both the regular and the `plasmid-based¿ senescence process. We show that the longevity trait is maternally inherited and coincides with the presence of a copy of the plasmid integrated in the 5¿ UTR of the mitochondrial Complex I genes nd2 and nd3. This mutation is associated with complex alterations in the respiratory chain, including a dispensable induction of the alternative oxidase. It is also associated with a stabilization of the mitochondrial chromosome and a reduction of the overall cellular level of reactive oxygen species.