Bresler S E, Kalinin V L, Suslova I N
Mol Gen Genet. 1982;188(1):111-4. doi: 10.1007/BF00333003.
Mutagenic action of 60Co gamma-rays on extracellular phages lambda red1 and lambda red113 after irradiation in 4% nutrient broth in the absence or in the presence of 0.1 M cysteamine or in dried samples was studied. The yield of c mutations was almost independent of the repair genotype of the host cells (uvrA6, polA1, recA13, lexA102, uvrE502, uvrD3 or xthA9), of the phage Red function and of the conditions of gamma-irradiation and was 1 . 10(-12) per base pair and 1 rad. When the SOS-repair system of the host cells was induced by moderate UV irradiation, the yield of c-mutations was drastically enhanced in phage irradiated in broth, but not in phage irradiated in the dried state. These data allow us to suppose that the direct action of gamma-rays induces, in phage DNA, premutational lesions that are fixed into mutations by replication. On the other hand after gamma-irradiation in broth, when indirect radiation effects are only partially suppressed, about 85% of premutational lesions are converted into mutations by means of the inducible, errorprone SOS-repair system.
研究了60Coγ射线在不存在或存在0.1M半胱胺的情况下于4%营养肉汤中辐照后，以及在干燥样品中辐照后对细胞外噬菌体λred1和λred113的诱变作用。c突变的发生率几乎与宿主细胞（uvrA6、polA1、recA13、lexA102、uvrE502、uvrD3或xthA9）的修复基因型、噬菌体的Red功能以及γ辐照条件无关，为每碱基对每拉德1.10(-12)。当宿主细胞的SOS修复系统由适度紫外线辐照诱导时，在肉汤中辐照的噬菌体中c突变的发生率急剧增加，但在干燥状态下辐照的噬菌体中则没有。这些数据使我们能够推测，γ射线的直接作用在噬菌体DNA中诱导了预突变损伤，这些损伤通过复制固定为突变。另一方面，在肉汤中进行γ辐照后，当间接辐射效应仅部分受到抑制时，约85%的预突变损伤通过可诱导的易错SOS修复系统转化为突变。
