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2017 Fiscal Year Final Research Report

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

Research Project

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Project/Area Number 15K18581
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Genetics/Chromosome dynamics
Research InstitutionThe 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
KeywordsDNA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

URL: 

Published: 2019-03-29  

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