GCN5 enables HSP12 induction promoting chromatin remodeling not histone acetylation

Regulation of stress responsive genes represents one of the best examples of gene induction and the relevance and involvement of different regulators may change for a given gene depending on the challenging stimulus. HSP12 gene is induced by very different stimuli, however the molecular response to the stress has been characterized in detail only for heat shock treatments. In this work we want to verify whether, the regulation of transcription induced by oxidative stress, utilizes the same epigenetic solutions relative to those employed in heat shock response. We also monitored HSP12 induction employing spermidine, a known acetyltransferase inhibitor, and observed an oxidative stress that synergizes with spermidine treatment. Our data show that during transcriptional response to H2O2, histone acetylation and chromatin remodeling occur. However, when the relevance of Gcn5p on these processes was studied, we observed that induction of transcription is GCN5 dependent and this does not rely on histone acetylation by Gcn5p despite its HAT activity. Chromatin remodeling accompanying gene activation is rather GCN5 dependent. Thus, GCN5 controls HSP12 transcription after H2O2 treatment by allowing chromatin remodeling and it is only partially involved in HSP12 histone acetylation regardless its HAT activity.