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A mitochondrial model for premature ageing of somatically cloned mammals.

作者信息

Allen J F, Allen C A

机构信息

Lund University, Sweden.

出版信息

IUBMB Life. 1999 Oct;48(4):369-72. doi: 10.1080/713803544.

DOI:10.1080/713803544
PMID:10632563
Abstract

Cloned sheep have recently been discovered to have an unexpectedly advanced biological age. We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cells but not to zygotes produced by fertilization in normal sexual reproduction. Each increment of ageing in cloning experiments is therefore predicted to be maternally inherited. The hypothesis suggests practical ways of decreasing the effect. The hypothesis is itself a prediction of the recent proposal that mitochondria of the female germ line function primarily as genetic templates.

摘要

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