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Only recently have scientists verified that mitochondria can repair their
DNA. Early observations had suggested that one reason why DNA damage accumulated
in mitochondria was that DNA defects were not removed. Mitochondrial DNA
does not generate any DNA repair proteins, but scientists at the University
of Pittsburgh Medical School have found that mitochondria are able to snip
out damaged segments quite well, and there are also indications of even
more complex repair processes. Mitochondrial DNA repair appears to be emerging
as an active area of research. In an article appearing in the 1999 Journal
of Cell Biology, a research team led by Dr. Jodi Nunnari at the University
of California, Davis, identified a previously unknown factor that assists
in repairing oxidatively damaged mitochondrial DNA.
A study of animal cells artificially exposed to oxidant stress revealed
that cells showing the most resistance to damage had a higher capacity
to repair their mitochondrial DNA. Resistant cells also appeared to be
naturally endowed with the ability to minimize initial damage to their
mitochondria. These results suggest that even after DNA damage occurs,
repair can rescue the mitochondria.
A team led by Dr. Simon Melov of the Buck Center for Research in Aging
in Novato, California, has developed a method for detecting mitochondrial
DNA mutations. Using this assay on aging human brain cells, they found
a mixed array of rearranged DNAs. The technique should have wider applications,
as scientists seek to pinpoint defects and mutations in mitochondrial
DNA that might be the result of oxidative damage.
Similar genetic techniques have already proved successful in locating
"hot-spots" in mitochondrial DNA - regions where defects and
mutations tend to cluster. Dr. Giuseppe Attardi and his research team
at the California Institute of Technology reported last year in the journal
Science that mutations in mitochondrial DNA were not widely distributed
in the DNA, but appeared to be clustered in so-called "control"
regions of the DNA that regulate the activity of mitochondrial genes.
One or more mutations appeared in an individual only at an advanced age.
Some mutations appeared in more than one individual. Most strikingly,
a DNA sequence rearrangement was found in a generally high proportion
of mitochondrial DNA molecules in individuals above 65 years of age, though
it was absent in younger individuals.
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