Abstract # 2392 The Identification of Mre11 as the Central Participant in Multiple Subpathways of Repairing Chromosomal Double-StrandBreak

Presenter: Zhuang, Jing

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We discovered that silencing of Mre11 protein expression using siRNA in HEK293 cells resulted in 2-fold suppression of HDR- but 3-4 fold increase of SSA-mediated repair of enzymatic chromosomal DSB, surprisingly, indicating that Mre11 differentially regulates the two subtypes of HR by promoting error-free HDR and suppressing deletional SSA. With regard to NHEJ, we found that loss of Mre11 has no effect on Ku-dependent C-NHEJ but resulted in 6 fold decrease of microhomology-mediated D-NHEJ, suggesting that Mre11 is required for error-prone D-NHEJ only. The differential effects of loss of Mre11 on DSB repair subpathways are not due to the cell cycle disturbance, since there was no significant change in cell cycle distribution in cells with or without silencing of Mre11. In consistent with previous report, inhibition of Mre11 by expressing siRNA in HEK293 cells leads to increased radiosensitivity.

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