The induction of rho− mutants by UV or γ-rays is independent of the nuclear recombinational repair pathway in Saccharomyces cerevisiae

Martine Heude
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引用次数: 3

Abstract

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.

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
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。
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