TY - JOUR
T1 - Maternal age effects on fecundity and offspring egg-to-adult viability are not affected by mitochondrial haplotype
AU - Koch, Rebecca Elizabeth
AU - Phillips, James
AU - Camus, Maria Florencia
AU - Dowling, Damian Kimon
PY - 2018/11
Y1 - 2018/11
N2 - While numerous studies have demonstrated that mitochondrial genetic variation can shape organismal phenotype, the level of contribution the mitochondrial genotype makes to life-history phenotype across the life course remains unknown. Furthermore, a clear technical bias has emerged in studies of mitochondrial effects on reproduction, with many studies conducted on males, but few on females. Here, we apply a classic prediction of the evolutionary theory of aging to the mitochondrial genome, predicting the declining force of natural selection with age will have facilitated the accumulation of mtDNA mutations that confer late-life effects on female reproductive performance. This should lead to increased levels of mitochondrial genetic variation on reproduction at later-life stages. We tested this hypothesis using thirteen strains of Drosophila melanogaster that each possessed a different mitochondrial haplotype in an otherwise standard nuclear genetic background. We measured fecundity and egg-to-adult viability of females over five different age classes ranging from early to late life and quantified the survival of females throughout this time period. We found no significant variation across mitochondrial haplotypes for the reproductive traits, and no mitochondrial effect on the slope of decline in these traits with increasing age. However, we observed that flies that died earlier in the experiment experienced steeper declines in the reproductive traits prior to death, and we also identified maternal and grandparental age effects on the measured traits. These results suggest the mitochondrial variation does not make a key contribution to shaping the reproductive performance of females.
AB - While numerous studies have demonstrated that mitochondrial genetic variation can shape organismal phenotype, the level of contribution the mitochondrial genotype makes to life-history phenotype across the life course remains unknown. Furthermore, a clear technical bias has emerged in studies of mitochondrial effects on reproduction, with many studies conducted on males, but few on females. Here, we apply a classic prediction of the evolutionary theory of aging to the mitochondrial genome, predicting the declining force of natural selection with age will have facilitated the accumulation of mtDNA mutations that confer late-life effects on female reproductive performance. This should lead to increased levels of mitochondrial genetic variation on reproduction at later-life stages. We tested this hypothesis using thirteen strains of Drosophila melanogaster that each possessed a different mitochondrial haplotype in an otherwise standard nuclear genetic background. We measured fecundity and egg-to-adult viability of females over five different age classes ranging from early to late life and quantified the survival of females throughout this time period. We found no significant variation across mitochondrial haplotypes for the reproductive traits, and no mitochondrial effect on the slope of decline in these traits with increasing age. However, we observed that flies that died earlier in the experiment experienced steeper declines in the reproductive traits prior to death, and we also identified maternal and grandparental age effects on the measured traits. These results suggest the mitochondrial variation does not make a key contribution to shaping the reproductive performance of females.
KW - aging
KW - Drosophila melanogaster
KW - evolution of aging
KW - mitochondrial genome
KW - mitonuclear
KW - mother's curse
KW - mtDNA
KW - reproduction
UR - http://www.scopus.com/inward/record.url?scp=85055686805&partnerID=8YFLogxK
U2 - 10.1002/ece3.4516
DO - 10.1002/ece3.4516
M3 - Article
AN - SCOPUS:85055686805
VL - 8
SP - 10722
EP - 10732
JO - Ecology and Evolution
JF - Ecology and Evolution
SN - 2045-7758
IS - 22
ER -