Kozhina T N, Evstiukhina T A, Peshekhonov V T, Chernenkov A Yu, Korolev V G
Genetika. 2016 Mar;52(3):300-10.
In the Saccharomyces cerevisiae yeasts, the DOT1 gene product provides methylation of lysine 79 (K79) of hi- stone H3 and the SET2 gene product provides the methylation of lysine 36 (K36) of the same histone. We determined that the dot1 and set2 mutants suppress the UV-induced mutagenesis to an equally high degree. The dot1 mutation demonstrated statistically higher sensitivity to the low doses of MMC than the wild type strain. The analysis of the interaction between the dot1 and rad52 mutations revealed a considerable level of spontaneous cell death in the double dot1 rad52 mutant. We observed strong suppression of the gamma-in- duced mutagenesis in the set2 mutant. We determined that the dot1 and set2 mutations decrease the sponta- neous mutagenesis rate in both single and d ouble mutants. The epistatic interaction between the dot1 and set2 mutations and almost similar sensitivity of the corresponding mutants to the different types of DNA damage allow one to conclude that both genes are involved in the control of the same DNA repair pathways, the ho- mologous-recombination-based and the postreplicative DNA repair.
在酿酒酵母中,DOT1基因产物负责组蛋白H3赖氨酸79(K79)的甲基化,而SET2基因产物负责同一组蛋白赖氨酸36(K36)的甲基化。我们确定dot1和set2突变体对紫外线诱导的诱变具有同等程度的抑制作用。dot1突变体对低剂量丝裂霉素C(MMC)的敏感性在统计学上高于野生型菌株。对dot1和rad52突变之间相互作用的分析表明,双突变体dot1 rad52中存在相当程度的自发细胞死亡。我们观察到set2突变体对γ射线诱导的诱变有强烈抑制作用。我们确定dot1和set2突变在单突变体和双突变体中均降低了自发诱变率。dot1和set2突变之间的上位性相互作用以及相应突变体对不同类型DNA损伤几乎相似的敏感性,使我们可以得出结论,这两个基因都参与了相同DNA修复途径的调控,即基于同源重组的修复和复制后DNA修复。