Use of the H2AX activation response to investigate DNA repair process

The cellular response to DNA damage and repair mechanism involves numerous signalings and effector pathways. One of the most well-established DNA damage marker is the phosphorylation of the histone H2AX (γ-H2AX). The γ-H2AX directly indicates the sites of DNA-double strand break (DSB) occurrences and their repairs. The cell cycle arrest is another response to DNA damage. The G2/M arrest is regulated by numerous proteins involved in DNA damage repair, such as MDM2 and p53 effector molecules. p53 is a tumor suppressor protein, which stimulates p21 for the decision of a cell to undergo cell-cycle arrest. These check-points during the cell cycle progression provide cells with sufficient time to repair the radiation-induced DNA damage. In this study, we identified various factors involved in DNA damage repair following high dose exposure of cells. In particular, we investigated whether H2AX phosphorylation has a dependence on cell cycle distribution. According to the observations in this study, the level of γ-H2AX may be perturbed by other repair factors of DNA damage, such as cell cycle arrest. We suggest that the γ-H2AX be carefully used as a DNA damage/repair marker.