Difference between revisions of "Brown 2012 Abstract Bioblast"
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|year=2012 | |year=2012 | ||
|event=[[Bioblast 2012]] | |event=[[Bioblast 2012]] | ||
|abstract=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.Β 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.Β 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.Β 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. | |abstract=[[File:GuyBrown.JPG|right|150px|Guy Brown]] | ||
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.Β 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.Β 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.Β 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 | |keywords=Aging, Mitochondrial genome | ||
|mipnetlab=UK Cambridge Brown GC | |mipnetlab=UK Cambridge Brown GC | ||
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{{Labeling | {{Labeling | ||
| | |area=mtDNA;mt-genetics, nDNA;cell genetics | ||
|organism=Human | |organism=Human | ||
|diseases=Aging;senescence | |||
|journal=Mitochondr Physiol Network | |journal=Mitochondr Physiol Network | ||
|articletype=Abstract | |articletype=Abstract | ||
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== Affiliations and author contributions == | == Affiliations and author contributions == | ||
Cellular Biochemistry | Cellular Biochemistry, University of Cambridge, UK, Email: [email protected] | ||
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University of Cambridge, UK | |||
== Help == | == Help == | ||
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Latest revision as of 17:15, 3 February 2016
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
Organism: Human
Affiliations and author contributions
Cellular Biochemistry, University of Cambridge, UK, Email: [email protected]