Analyzing the mechanism of recombination-dependent replication restart in eukaryotes

Research Project

Project/Area Number	24770170
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Molecular biology
Research Institution	Tokyo University of Pharmacy and Life Science
Principal Investigator	HASHIMOTO Yoshitami 東京薬科大学, 生命科学部, 助教 (50616761)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000) Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords	DNA複製フォーク / レプリソーム / 組換え / リン酸化 / アフリカツメガエル卵無細胞系 / GINS / ATR/ATM / Rad51 / CMGヘリカーゼ / ATM/ATR / 組換え修復 / 複製ストレス / ニワトリDT40細胞 / アフリカツメガエル卵抽出液 / 複製再開 / DNA損傷
Outline of Final Research Achievements	A replication fork collapsed by a break in the template DNA can be rescued by a recombination-mediated pathway, allowing the re-establishment of a functional replication fork. However, it is not well understood how the replisome components are regulated during fork collapse and restart. In this study, I found that Psf2, a subunit of GINS (a replisome factor), is phosphorylated by ATR/ATM upon fork arrest, which is involved in the replication restart.