Mechanisms for Ubiquitination-Dependent Regulation of Homologous Recombination

2014 Fiscal Year Final Research Report

• Project/Area Number: 23310040
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Risk sciences of radiation/Chemicals
• Research Institution: Osaka University (2012-2013); Keio University (2011)
• Principal Investigator: NAKADA Shinichiro 大阪大学, 医学(系)研究科(研究院), 准教授 (70548528)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: DNA損傷応答 / DNA修復 / ユビキチン / 相同組換え修復

Outline of Final Research Achievements

DNA double-strand breaks (DSBs) are repaired by the error-free homologous recombination pathway and error-prone non-homologous end joining. Ubiquitination is indispensable post-translational modification for DSB response. Here, we focused on the mechanism of BRCA1-independent HR and ubiquitination-dependent regulation of HR. In this research project, we found that E3 ubiquitin ligase RNF8 regulates RAD51 assembly at DSB sites in the absence of BRCA1 and 53BP1. We also found that deubiquitinating enzyme OTUB2 finely regulates DSB-induced ubiquitination and enables HR.

Free Research Field

DNA損傷応答