Applying the genetic theories of ageing to the cytoplasm: cytoplasmic genetic covariation for fitness and lifespan

Two genetic models exist to explain the evolution of ageing - mutation accumulation (MA) and antagonistic pleiotropy (AP). Under MA, a reduced intensity of selection with age results in accumulation of late-acting deleterious mutations. Under AP, late-acting deleterious mutations accumulate because...

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Bibliographic Details
Published in:Journal of evolutionary biology 2009-04, Vol.22 (4), p.818-827
Main Authors: DOWLING, D.K, MAKLAKOV, A.A, FRIBERG, U, HAILER, F
Format: Article
Language:English
Subjects:
ageing
Aging
Aging - physiology
Animals
antagonistic pleiotropy
Biologi
Biology
Cytoplasm
Cytoplasm - genetics
DNA, Mitochondrial - genetics
Drosophila melanogaster
Drosophila melanogaster - genetics
Drosophila melanogaster - physiology
Evolutionary biology
Female
Genetic Variation
Genetics
Insects
Longevity - physiology
mitochondria
mitochondrial DNA
mtDNA
Mutation
mutation accumulation
NATURAL SCIENCES
NATURVETENSKAP
Reproduction - physiology
senescence
Time Factors
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Summary:Two genetic models exist to explain the evolution of ageing - mutation accumulation (MA) and antagonistic pleiotropy (AP). Under MA, a reduced intensity of selection with age results in accumulation of late-acting deleterious mutations. Under AP, late-acting deleterious mutations accumulate because they confer beneficial effects early in life. Recent studies suggest that the mitochondrial genome is a major player in ageing. It therefore seems plausible that the MA and AP models will be relevant to genomes within the cytoplasm. This possibility has not been considered previously. We explore whether patterns of covariation between fitness and ageing across 25 cytoplasmic lines, sampled from a population of Drosophila melanogaster, are consistent with the genetic associations predicted under MA or AP. We find negative covariation for fitness and the rate of ageing, and positive covariation for fitness and lifespan. Notably, the direction of these associations is opposite to that typically predicted under AP.
ISSN:1010-061X
1420-9101
1420-9101
DOI:10.1111/j.1420-9101.2009.01692.x