Rescue of arrested replication forks by multiple ubiquitination of PCNA

2016 Fiscal Year Final Research Report

• Project/Area Number: 26740017
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Nagoya University
• Principal Investigator: Kanao Rie 名古屋大学, 環境医学研究所, 助教 (30542287)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: DNA損傷トレランス / PCNA / モノユビキチン化 / 損傷乗り越え複製

Outline of Final Research Achievements

DNA damage tolerance is an important mechanism to prevent DNA replication arrest by DNA damage. It is suggested that DNA damage tolerance is regulated by post-translational modifications of PCNA at K164. PCNA forms a ring-shaped structure consist of homo-trimeric PCNA molecules, which means a single PCNA ring have three modifiable K164. In this study, I investigated the mechanism of DNA damage tolerance pathway which is regulated by simultaneously mono-ubiquitinated PCNA on three K164 in a ring. I analyzed the responses of the cells expressing ectopic PCNA mutated at K164 to DNA damaging agents.

Free Research Field

DNA修復