Submission Title

Elucidating the role of Exo1 and Mre11 mutations in DNA damage response

Location

Jereld R. Nicholson Library: Grand Avenue

Subject Area

Biology

Description

DNA double strand breaks (DSBs) are one of the most deleterious types of DNA damage that cells combat. DSBs are processed by the 3′-to-5′ exonuclease activity of the DSB repair nuclease, Mre11, to generate protruding 3′ single stranded DNA (ssDNA) at DSBs. Exonuclease 1 (EXO1) is an evolutionarily, well-conserved exonuclease. Its ability to resect DNA in the 5′-3′ direction has been extensively characterized and shown to be implicated in several genomic DNA metabolic processes such as replication stress response, double strand break repair (DSBR), mismatch repair, nucleotide excision repair and telomere maintenance. Both Mre11 and Exo1 play a critical role in the DNA resection in DSBR. Mre11 is responsible for the initial short-range resection, which is followed by the long resection by Exo1 before strand invasion in DSBR. However, the regulation of this switch between Mre11 and Exo1 is not well understood. The purpose of this study is to test the hypothesis that EXO1 and MRE11 gene variants contribute to genomic instability by aberrant DNA repair. This project seeks to understand the potential role of disease-associated variants of Exo1 and Mre11 in defective resection function, thus inducing genomic instability.

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May 20th, 9:00 AM May 20th, 3:00 PM

Elucidating the role of Exo1 and Mre11 mutations in DNA damage response

Jereld R. Nicholson Library: Grand Avenue

DNA double strand breaks (DSBs) are one of the most deleterious types of DNA damage that cells combat. DSBs are processed by the 3′-to-5′ exonuclease activity of the DSB repair nuclease, Mre11, to generate protruding 3′ single stranded DNA (ssDNA) at DSBs. Exonuclease 1 (EXO1) is an evolutionarily, well-conserved exonuclease. Its ability to resect DNA in the 5′-3′ direction has been extensively characterized and shown to be implicated in several genomic DNA metabolic processes such as replication stress response, double strand break repair (DSBR), mismatch repair, nucleotide excision repair and telomere maintenance. Both Mre11 and Exo1 play a critical role in the DNA resection in DSBR. Mre11 is responsible for the initial short-range resection, which is followed by the long resection by Exo1 before strand invasion in DSBR. However, the regulation of this switch between Mre11 and Exo1 is not well understood. The purpose of this study is to test the hypothesis that EXO1 and MRE11 gene variants contribute to genomic instability by aberrant DNA repair. This project seeks to understand the potential role of disease-associated variants of Exo1 and Mre11 in defective resection function, thus inducing genomic instability.