Difference between revisions of "Brown 2012 Abstract Bioblast"
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Revision as of 15:37, 18 November 2014
Brown GC (2012) Low selective pressure on our mitochondrial genome may explain its rapid evolution, poor adaption and our aging. Mitochondr Physiol Network 17.12. |
Link: MiPNet17.12 Bioblast 2012 - Open Access
Brown GC (2012)
Event: Bioblast 2012
There is a much lower effective selective pressure on our mitochondrial genome relative to nuclear-encoded mitochondrial genes because the mitochondrial genome: 1) is present at high copy numbers per cells, 2) does not undergo recombination; 3) is selected in females only, and 4) is not selected by the sperm race. In addition, the mitochondrial genome may mutate at a higher rate. The large mismatch between mitochondrial and nuclear genes in the ability of evolution to select beneficial and eliminate detrimental variants might be a cause of the rapid evolution and poor adaption of mitochondrial genes. As mammals and humans became larger, brainier, with more skills to pass on and delayed sexual-maturity, and decreased extrinsic causes of death, there would have been selection pressure to delay ageing and age-related disease. But that selection pressure would have had relatively little effect on the mitochondrial relative to nuclear genome, causing mitochondria to be a major contributor to aging.
β’ Keywords: Aging, Mitochondrial genome
β’ O2k-Network Lab: UK Cambridge Brown GC
Labels: MiParea: mtDNA;mt-genetics, nDNA;cell genetics Pathology: Aging; senescence"Aging; senescence" is not in the list (Aging;senescence, Alzheimer's, Autism, Cancer, Cardiovascular, COPD, Diabetes, Inherited, Infectious, Myopathy, ...) of allowed values for the "Diseases" property.
Organism: Human
Affiliations and author contributions
Cellular Biochemistry, University of Cambridge, UK, Email: [email protected]