Faculty Advisor

Adams, David S.

Abstract

The Fanconi Anemia pathway is a complex DNA damage response which combines translesion synthesis and homologous recombination to repair DNA interstrand crosslinks. Mutations in any of the fifteen known FA genes, such as Fancd2, result in widespread chromosomal instability and the formation of radial chromosome structures. We considered the hypothesis that proteins of the mismatch repair pathway contribute to this genomic instability since MMR proteins bind ICLs to induce DNA breaks. This MQP presents evidence that Msh2 depletion mitigates the formation of radial chromosomes in Fancd2-deficient cells. In addition, we show that Msh2 depletion reduces cellular sensitivity to crosslinking agents such as Mitomycin C, and suppresses the ATM/ATR checkpoint response.

Publisher

Worcester Polytechnic Institute

Date Accepted

April 2013

Major

Biology and Biotechnology

Project Type

Major Qualifying Project

Accessibility

Unrestricted

Advisor Department

Biology and Biotechnology

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