Understanding the mechanisms by which Ctf4 protein promotes proper repair of DSBs formed upon inhibition of rDNA replication

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K18581
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Genetics/Chromosome dynamics
• Research Institution: The University of Tokyo
• Principal Investigator: Sasaki Mariko 東京大学, 分子細胞生物学研究所, 助教 (50722013)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: DNA複製阻害 / DNA二重鎖切断 / Ctf4 / ゲノム再編成 / rDNA / ゲノム不安定化

Outline of Final Research Achievements

In this study, I aimed to understand the mechanisms by which Ctf4 protein functions to promote proper repair of DNA double-strand breaks (DSBs) at the arrested replication forks. It has been believed that DSBs at arrested forks are repaired by homologous recombination, which is required for repair of DSBs formed in the G2/M phases of the cell cycle. However, I found that DSBs at arrested forks are repaired by the novel pathways that are independent of homologous recombination. I also showed that Ctf4 protein, a component of replication machineries, plays an important role for proper repair of DSBs at arrested forks, by suppressing the initiation of homologous recombination upon DSB formation.

Free Research Field

分子生物学