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No sex please, we're mitochondria: a hypothesis on the somatic unit of inheritance of mammalian mtDNA
Author(s) -
Jacobs Howard T.,
Lehtinen Sanna K.,
Spelbrink Johannes N.
Publication year - 2000
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(200006)22:6<564::aid-bies9>3.0.co;2-4
Subject(s) - heteroplasmy , mitochondrial dna , nucleoid , biology , somatic cell , genetics , mitosis , mitochondrion , cell division , complementation , mutation , mutant , microbiology and biotechnology , cell , gene , escherichia coli
Abstract In this article we develop a model for the organization and maintenance of mitochondrial DNA (mtDNA) in mammalian somatic cells, based on the idea that the unit of genetic function comprises a group of mtDNA molecules that are semi‐permanently associated as a mitochondrial nucleoid. Different mtDNA molecules within a nucleoid need not be genetically identical. We propose that nucleoids replicate faithfully via a kind of mitochondrial mitosis, generating daughter nucleoids that are identical copies of each other, but which can themselves segregate freely. This model can account for the very slow rates of mitotic segregation observed in cultured, heteroplasmic cell‐lines, and also for the apparently poor complementation observed between different mutant mtDNAs co‐introduced into ρ 0 cells (cells that lack endogenous mtDNA). It also provides a potential system for maintaining the mitochondrial genetic fitness of stem cells in the face of a presumed high somatic mutation rate of mtDNA and many rounds of cell division in the absence of phenotypic selection. BioEssays 22:564–572, 2000. © 2000 John Wiley & Sons, Inc.