Brown 2012 Abstract Bioblast

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.

• Keywords: Aging, Mitochondrial genome

• O2k-Network Lab: UK Cambridge Brown GC

Labels:

Stress:Aging; Senescence"Aging; Senescence" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Human, Other Mammal"Other Mammal" is not in the list (Human, Pig, Mouse, Rat, Guinea pig, Bovines, Horse, Dog, Rabbit, Cat, ...) of allowed values for the "Mammal and model" property. 

Affiliations and author contributions

Cellular Biochemistry, University of Cambridge, UK, Email: [email protected]

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