title: Intracellular evolution of mitochondrial DNA (mtDNA) and the tragedy of the cytoplasmic commons.
abstract: Mitochondria exist in large numbers per cell. Therefore, the strength of natural selection on individual mtDNAs for their contribution to cellular fitness is weak whereas the strength of selection in favor of mtDNAs that increase their own replication without regard for cellular functions is strong. This problem has been solved for most mitochondrial genes by their transfer to the nucleus but a few critical genes remain encoded by mtDNA. Organisms manage the evolution of mtDNA to prevent mutational decay of essential services mitochondria provide to their hosts. Bottlenecks of mitochondrial numbers in female germlines increase the homogeneity of mtDNAs within cells and allow intraorganismal selection to eliminate cells with low quality mitochondria. Mechanisms of intracellular "quality control" allow direct selection on the competence of individual mtDNAs. These processes maintain the integrity of mtDNAs within the germline but are inadequate to indefinitely maintain mitochondrial function in somatic cells.
authors.affiliation: Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA, USA.
authors.forename: David
authors.initials: D
authors.lastname: Haig
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D005075:Biological Evolution; D004272:DNA, Mitochondrial; D005260:Female; D006801:Humans; D008928:Mitochondria / Q000235:genetics* / Q000502:physiology; D063306:Mitophagy; D009154:Mutation; D010063:Ovum
chemical_list: D004272:DNA, Mitochondrial
keywords: aging; apoptosis; bottleneck; mitochondria; mitophagy; mtDNA; public goods