Gracheva L M, Evstiukhina T A, Koval'tsova S V, Fedorova I V, Korolev V G
Genetika. 1996 Jul;32(7):922-6.
During recent years, genes controlling mutation in higher eukaryotes have been found to be involved actively in carcinoma regeneration in cells. In this respect, studying the genetic control of mutagenesis becomes a key direction of research into mechanisms responsible for cancer generation. The results of studying interaction of mutations in the HSM3 and HSM6 genes, controlling spontaneous and induced mutagenesis in yeasts, and mutations impairing three known pathways of DNA damage repair in this microorganism, are described in this work. It was shown that mutation rev3 completely blocks UV-induced mutagenesis in all mutants studied. On the other hand, mutation rad2 synergistically interacts with mutations him1, hsm1, hsm3, hsm6, and hsm2, thus enhancing the frequency of UV-induced mutagenesis in double mutants multiple times. Mutations him2 and him3 manifested epistatic interaction with mutation rad2. With mutation rad54, the interaction was epistatic for mutations him1 and hsm2 and was additive for mutations hsm1, him2, and him3. On the basis of the data obtained, we developed a scheme for the appearance of mismatch bases in the process of repair of UV-induced DNA damage.
近年来，已发现控制高等真核生物突变的基因积极参与细胞中的癌再生。在这方面，研究诱变的遗传控制成为癌症发生机制研究的一个关键方向。本文描述了研究酵母中控制自发和诱导诱变的HSM3和HSM6基因中的突变与该微生物中损害三种已知DNA损伤修复途径的突变之间相互作用的结果。结果表明，rev3突变在所有研究的突变体中完全阻断紫外线诱导的诱变。另一方面，rad2突变与him1、hsm1、hsm3、hsm6和hsm2突变协同相互作用，从而使双突变体中紫外线诱导的诱变频率提高数倍。him2和him3突变与rad2突变表现出上位性相互作用。对于rad54突变，与him1和hsm2突变的相互作用是上位性的，与hsm1、him2和him3突变的相互作用是加性的。基于所获得的数据，我们制定了紫外线诱导的DNA损伤修复过程中错配碱基出现的方案。
