E-GEOD-12046 - Expression profiles and ChIP on chip genomewide experiments with R2G mutant virus
Submitted on 8 July 2008, released on 26 August 2008, last updated on 3 May 2014
Adenovirus e1a induces quiescent human cells to divide. We found that e1a causes global relocalization of the RB-proteins (RB, p130, p107) and p300/CBP histone acetyltransferases on promoters that restricts H3K18ac to a limited set of genes to stimulate cell cycling and inhibit antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to cell cycle/growth genes, causing enrichment of p300/CBP, PCAF, H3K18ac, depletion of RB-proteins, and transcriptional activation. e1a also associates transiently with antiviral genes, causing enrichment for RB, p130, H4K16ac, increased nucleosome density, and repression. At later times, e1a and p107 bind mainly to development/differentiation genes, repressing transcription. The temporal order of e1a binding required its interactions with p300/CBP and RB-proteins. Our data uncover a defined transcriptional and epigenetic reprogramming leading to cellular transformation. Expression profiles and ChIP on chip genomewide experiments with R2G mutant virus (expressing a mutated version of small e1a).
transcription profiling by array, ChIP-chip by tiling array
Siavash K Kurdistani <Skurdistani@mednet.ucla.edu>, Arnold Berk, Gregory Horwitz, Matteo Pellegrini, Roberto Ferrari, Siavash Kurdistani, Wei Xei
Epigenetic reprogramming by adenovirus e1a. Ferrari R, Pellegrini M, Horwitz GA, Xie W, Berk AJ, Kurdistani SK.