Dot1 and Set2 histone methylases control the spontaneous and UV-induced mutagenesis levels in the Saccharomyces cerevisiae yeasts

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• 作者：T. N. Kozhina ; T. A. Evstiukhina ; V. T. Peshekhonov…
• 关键词：yeasts ; DNA repair ; mutagenesis ; methylation ; chromatin ; DOT1 ; SET2
• 刊名：Russian Journal of Genetics
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：52
• 期：3
• 页码：263-272
• 全文大小：491 KB
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• 作者单位：T. N. Kozhina (1) (2)
  T. A. Evstiukhina (1)
  V. T. Peshekhonov (1)
  A. Yu. Chernenkov (1)
  V. G. Korolev (1)
  
  1. Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, St. Petersburg, Gatchina, Leningrad oblast, 188300, Russia
  2. Department of Biophysics, Institute of Physics, Nanotechnology, and Telecommunications, St. Petersburg State Polytechnic University, St. Petersburg, 195251, Russia
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Human Genetics
  Animal Genetics and Genomics
  Microbial Genetics and Genomics
  Russian Library of Science
  
• 出版者：MAIK Nauka/Interperiodica distributed exclusively by Springer Science+Business Media LLC.
• ISSN：1608-3369

文摘

In the Saccharomyces cerevisiae yeasts, the DOT1 gene product provides methylation of lysine 79 (K79) of histone 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-induced mutagenesis in the set2 mutant. We determined that the dot1 and set2 mutations decrease the spontaneous mutagenesis rate in both single and double 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 homologous-recombination-based and the postreplicative DNA repair.