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What the papers say: Where is the somatic mutation that causes aging?
Author(s) -
Driver Christopher
Publication year - 2004
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/bies.20149
Subject(s) - mitochondrial dna , somatic cell , biology , genetics , gene , mutation , nuclear gene , mitochondrion , oxidative damage , function (biology) , dna damage , nuclear dna , dna , oxidative stress , biochemistry
It has been proposed that somatic mutations make major contributions to aging. The first paper, based on a gene knock‐in mouse, supports a contributory role for mutation in mtDNA1 in aging, but does not support a damaged‐mtDNA‐producing‐more‐damaged‐mtDNA hypothesis.1 The second paper2 indicates some GC‐rich sequences in the nuclear DNA are more sensitive to oxidative damage than mtDNA. As a result, key genes involved in brain function and mitochondrial function are progressively inactivated with age. Failure in these nucleus‐encoded mitochondrial genes may be a primary reason for mitochondrial failure in old age. BioEssays 26:1160–1163, 2004. © 2004 Wiley Periodicals, Inc.