Recruitment of healthy mitochondria fuels transmissible cancers.
The replication of mitochondrial DNA (mtDNA) is not under strict control of the nucleus. Therefore, within-cell selection can favour mtDNA variants with a replication or survival advantage even if deleterious for the cell. Here, we consider how the balance between selection within and among cells is shifted in cancer cell lineages, and how this affects the somatic evolution of mitochondria. Cancer cell lineages are known to be prone to mitochondrial genetic erosion. Nevertheless, some cancer lineages are long lived and a few exceptional lineages even can survive their host because of horizontal transmission to other individuals. Recent work now shows that such transmissible cancer cell lineages occasionally secondarily recruit the mitochondrial genome of their host, which we propose as a means to replace genetically eroded mitochondrial genomes. Studying the dynamics of the horizontal exchange of mtDNA between somatic cells may provide important insight into the evolution of mitochondria during somatic growth and in mitochondrial diseases.
Laboratory of Genetics, Wageningen University, The Netherlands. duur.aanen@wur.nl
Duur K
DK
Aanen
Marc F P M
MF
Maas
D000818:Animals; D019070:Cell Lineage; D004272:DNA, Mitochondrial / Q000235:genetics*; D054629:Genome, Mitochondrial; D006801:Humans; D008928:Mitochondria / Q000235:genetics*; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology*
D004272:DNA, Mitochondrial