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.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Puishys, Robert Edward

Contributors

• Cantor, Sharon

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-042313-131542

Advisor

• Adams, David S.

Year

• 2013

Sponsor

• UMass Medical School

Date created

• 2013-04-23

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright