在酿酒酵母中,紫外线或γ射线诱导的rho -突变体与核重组修复途径无关

Martine Heude
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引用次数: 3

摘要

为了发现核重组修复途径是否也作用于线粒体DNA (mtDNA)诱导的病变,研究了RAD50、- 51、- 52、- 55和- 56基因在辐射诱导rho -突变体中的可能作用。这种诱导似乎独立于这一途径。然而,在γ辐照的rad52二倍体中观察到呼吸缺陷突变体的有效诱导。我们证明这些突变不是由于缺乏mtDNA修复,而是由于γ射线引起的染色体损失。在未辐照的RAD+ cdc6二倍体在限制温度下培养的非整倍体后代中,有效地观察到染色体损失对二倍体呼吸能力的损害。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The induction of rho− mutants by UV or γ-rays is independent of the nuclear recombinational repair pathway in Saccharomyces cerevisiae

In order to discover whether the nuclear recombinational repair pathway also acts on lesions induced in mitochondrial DNA (mtDNA), the possible role of the RAD50, −51, −52, −55 and −56 genes on the induction of rho mutants by radiations was studied. Such induction appeared to be independent of this pathway. Nevertheless, an efficient induction of respiration-deficient mutants was observed in γ-irradiated rad52 diploids. We demonstrate that these mutants do not result from a lack of mtDNA repair, but from chromosome losses induced by γ-rays. Such an impairment of the respiratory ability of diploids by chromosome losses was effectively observed in the aneuploid progeny of unirradiated RAD+ cdc6 diploids incubated at the restrictive temperature.

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