Oct 29, 2008 - Snyder, E. Y., Deitcher, D. L., Walsh, C., Arnold-Aldea, S.,. Hartwieg, E. A. and Cepko, C. L. (1992) Multipotent neural cell lines can engraft and ...
Mutagenesis vol. 24 no. 2 pp. 161–167, 2009 Advance Access Publication 8 December 2008
doi:10.1093/mutage/gen064
Histone H2AX phosphorylation in response to changes in chromatin structure induced by altered osmolarity
Jennifer Baure, Atefeh Izadi1, Vannina Suarez1, Erich Giedzinski1, James E. Cleaver2, John R. Fike and Charles L. Limoli1,* Department of Neurological Surgery, University of California, San Francisco, CA 94110, USA, 1Department of Radiation Oncology, University of California, Irvine Medical Sciences I, Room B-149, Irvine, CA 92697-2695, USA and 2Auerback Melanoma Laboratory, UCSF Cancer Center, University of California, San Francisco, CA 94143, USA
DNA strand breaks trigger marked phosphorylation of histone H2AX (i.e. g-H2AX). While DNA double-strand breaks (DSBs) provide a strong stimulus for this event, the accompanying structural alterations in chromatin may represent the actual signal that elicits g-H2AX. Our data show that changes in chromatin structure are sufficient to elicit extensive g-H2AX formation in the relative absence of DNA strand breaks. Cells subjected to hypotonic (0.05 M) treatment exhibit g-H2AX levels that are equivalent to those found after the induction of 80–200 DNA DSBs (i.e. 2–5 Gy). Despite this significant increase in phosphorylation, cell survival remains relatively unaffected (
