|Budget Amount *help
¥170,690,000 (Direct Cost: ¥131,300,000、Indirect Cost: ¥39,390,000)
Fiscal Year 2013: ¥31,330,000 (Direct Cost: ¥24,100,000、Indirect Cost: ¥7,230,000)
Fiscal Year 2012: ¥31,330,000 (Direct Cost: ¥24,100,000、Indirect Cost: ¥7,230,000)
Fiscal Year 2011: ¥33,020,000 (Direct Cost: ¥25,400,000、Indirect Cost: ¥7,620,000)
Fiscal Year 2010: ¥33,020,000 (Direct Cost: ¥25,400,000、Indirect Cost: ¥7,620,000)
Fiscal Year 2009: ¥41,990,000 (Direct Cost: ¥32,300,000、Indirect Cost: ¥9,690,000)
Degeneration of homologous DNA recombination causes cancer and other diseases. We studied the functions of intrinsically disordered regions (IDRs) of Rad52 and Srs2, and their interactions with a RecA-family recombinase, Rad51, and other related proteins. Using mutagenesis, we identified amino acid-residues in the IDRs of Rad52 and Srs2, which are involved in the interaction with Rad51. A key finding from these studies is that Srs2 functions to facilitate the accurate repair of double-strand breaks without loss of heterozygosity in diploid mitotic cells. Our results further suggest a revision of double-strand-break repair model first proposed Szostak et al (1983). The proposed model includes the repair DNA synthesis-free capture of the processed single-strand DNA tail from the second end of the same double-strand break (Miura et al. PNAS 2013).