Defining the molecular mechanism of the cell cycle-specific regulation of chromosome end fusion at dysfunctional telomeres

2016 Fiscal Year Final Research Report

• Project/Area Number: 25440080
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cell biology
• Research Institution: Gunma University
• Principal Investigator: Konishi Akimitsu 群馬大学, 大学院医学系研究科, 講師 (50381877)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: テロメア / 染色体不安定化 / DNA損傷反応 / DNA修復 / 細胞周期

Outline of Final Research Achievements

In this study, we aimed to elucidate the molecular mechanism of the cell cycle-specific regulation of chromosome end fusion leading to the cell carcinogenesis. We revealed that chromatin ubiquitination at the end of chromosomes induced by telomere dysfunction was largely diminished in S/G2 cell cycle phase. As a result, the recruitment of 53BP1, which is an essential factor for chromosome end fusion, is suppressed in S/G2 phase. We also elucidated that TRF2, the central factor for telomere protection, directly binds to the chromatin (core histone) to stabilize the chromosome ends.

Free Research Field

細胞生物学