PARENT SESSION
1:30 PM to 3:30 PM
Monday, April 22, 2002
Poster Session 15 DNA Damage and Repair II
Room: Nevada Exhibition Center
(P20-204) Constitutive expression of acetylated p53 in AT Fibroblasts.
Song, Kyung*,1, Dritschilo, Anatoly1, Jung, Mira1, 1 Department of Radiation Medicine, Washington, DC
ABSTRACT-
AT cells exhibit abnormalities of cell cycle regulation and DNA damage repair process. The atm gene product that is mutated in patients with ataxia-telangiectasia appears to be a sensor for cellular response to genotoxic agents, including ionizing radiation, radiomimmetics and oxidative stress. Accumulated evidence suggests that the chromatin structure modification is not properly operated in these cells. However, the mechanism by which ATM involves in such signaling is not well understood. Previously, we have shown that ATM interacts with histone deaceylase 1 (HDAC1) and its complex exhibits histone deacetylase activity in response to ionizing radiation. In this study, we observed that AT fibroblasts are far more sensitive to micrococcal endonuclease digestion and exhibit an abundant basal level of acetylated p53 as compared to those of normal fibroblast controls. Furthermore, when ATM was expressed in AT cells, acetylated p53 was significantly reduced. Taken together, the data further confirm our previous finding showing an involvement of ATM in chromatin modification.
KEYWORDS: ATM, acetylated p53, micrococcal digestion , chromatin modification