Heude M
Institut Curie-Biologie, Centre Universitaire, Orsay, France.
Mutat Res. 1988 Sep;194(2):151-63. doi: 10.1016/0167-8817(88)90017-x.
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 gamma-irradiated rad52 diploids. We demonstrate that these mutants do not result from a lack of mtDNA repair, but from chromosome losses induced by gamma-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.
为了探究细胞核重组修复途径是否也作用于线粒体DNA(mtDNA)中诱导产生的损伤,我们研究了RAD50、-51、-52、-55和-56基因在辐射诱导ρ-突变体产生过程中的可能作用。这种诱导似乎与该途径无关。然而,在经γ射线照射的rad52二倍体中观察到了呼吸缺陷型突变体的有效诱导。我们证明这些突变体并非源于mtDNA修复的缺乏,而是由γ射线诱导的染色体丢失所致。在限制温度下培养的未照射RAD+ cdc6二倍体的非整倍体后代中,确实观察到了因染色体丢失而导致的二倍体呼吸能力受损。