Intracellular evolution of mitochondrial DNA (mtDNA) and the tragedy of the cytoplasmic commons. (8th April 2016)

• Record Type: Journal Article
• Authors: Haig, David
• Is Part Of: BioEssays. Volume 38:Number 6(2016:Jun.)
• Page Start: 549
• Page End: 555
• Publication Date: 2016-04-08
• Subjects: aging -- apoptosis -- bottleneck -- mitochondria -- mitophagy -- mtDNA -- public goods; Molecular biology -- Periodicals; Cytology -- Periodicals; Developmental biology -- Periodicals; 572.8
• DOI: 10.1002/bies.201600003
• Languages: English
• ISSNs: 0265-9247

Abstract

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. Abstract : Mitochondria are domesticated prokaryotes that reside in large herds within cells. Female germ cells are the stud farms that stock the herds of the next generation of bodies. Mechanisms of quality control within cells and selection among oogonia and oocytes are the mechanisms of "selective breeding" that maintain herd quality.