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- 조회 242
- 작성자 이태화
[2014 Spring Life Sciences & IBB Regular Seminar]
▶Subject: Lagging DNA Synthesis and Genome Stability-Rad52/Rad59-dependent recombination as a means to rectify faulty Okazaki fragment processing
▶Speaker: Yeon-Soo Seo, Ph.D. (KAIST)
▶Place: Auditorium(1F), Postech Biotech Center
Processing of Okazaki fragments during lagging strand DNA synthesis is closely associated with genome instability since many genes required for genome stability work together with DNA2, an essential processing enzyme. In this study, we identified RAD52 as a multicopy suppressor of the lethal helicase-negative dna2-K1080E allele. In contrast, Rad51 that works conjointly with Rad52 in homologous recombination failed to suppress dna2-K1080E, indicating a unique role(s) of Rad52 in the repair of faulty processing of Okazaki fragments. Rad52-QDDD/AAAA, a mutant defective in binding replication protein A and hence lacking the recombination mediator activity, did not rescue the lethality of dna2-K1080E. Furthermore, point mutations in Rad52 that abolish DNA anneal activity and its ability to interact with Rad59 also resulted in the failure in suppression. Our findings suggest that a Rad52/Rad59-dependent, but Rad51-independent recombination pathway can function to repair unprocessed flaps that have escaped endonucleolytic cleavage by Dna2.
▶Inquiry: Prof. Joo-Yeon Yoo (279-2346)
* This seminar will be given in English