Literature DB >> 19594330

How is mutant mitochondrial DNA clonally amplified? Much new evidence, still no answers.

Aubrey D N J de Grey1.   

Abstract

Twenty years have passed since Kadenbach and Müller-Höcker first proposed that the age-related accumulation of mutant mitochondrial DNA is caused by its clonal expansion, rather than by a "vicious cycle" of de novo mutational events caused by the disruptive metabolic impact of prior ones. Proof that they were correct emerged rapidly (though recognition of this was much slower); however, the mechanism underlying this selective advantage remained obscure. Numerous hypotheses were advanced during the 1990s, but proved hard to test. A wealth of data has been published very recently that bears on this question. While these reports surely bring us closer to an understanding of this phenomenon, and thus probably to a better understanding of how it might be combated or even reversed, they currently raise more questions than they answer.

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Year:  2009        PMID: 19594330     DOI: 10.1089/rej.2009.0879

Source DB:  PubMed          Journal:  Rejuvenation Res        ISSN: 1549-1684            Impact factor:   4.663


  2 in total

1.  Oxidative stress is not a major contributor to somatic mitochondrial DNA mutations.

Authors:  Leslie S Itsara; Scott R Kennedy; Edward J Fox; Selina Yu; Joshua J Hewitt; Monica Sanchez-Contreras; Fernando Cardozo-Pelaez; Leo J Pallanck
Journal:  PLoS Genet       Date:  2014-02-06       Impact factor: 5.917

2.  Targeted enrichment and high-resolution digital profiling of mitochondrial DNA deletions in human brain.

Authors:  Sean D Taylor; Nolan G Ericson; Joshua N Burton; Tomas A Prolla; John R Silber; Jay Shendure; Jason H Bielas
Journal:  Aging Cell       Date:  2013-09-11       Impact factor: 9.304

  2 in total

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