Fig. 8: Model of ATRX and DAXX-dependent effects on chromatin accessibility at p53-response elements and telomeres.
From: DAXX-ATRX regulation of p53 chromatin binding and DNA damage response
ATRX and DAXX loss of function mutations lead to a change in p53 chromatin binding and protein stability in U87 glioblastoma cell model. Loss of ATRX or DAXX reduces p53 chromatin binding and transcriptional activation of DNA-damage response genes, such as GADD45A and p21 and aberrant DNA-damage response (DDR). This correlated with a loss of H3.3 binding and accumulation of γH2AX at many loci, including p53-response elements and subtelomeres. Chromatin accessibility was decreased at p53 sites, but increased at telomere repeat DNA, along with loss of telomere T-loops (C-circle formation) and DNA-damage-associated telomere foci (APBs).
