GCN5 enables HSP12 induction promoting chromatin remodeling, not histone acetylation

Regulation of stress-responsive genes represent 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. The HSP12 gene is induced by very different stimuli; however, the molecular response to stress has been characterized in detail only for heat shock treatments. In this study, we aimed to verify whether the regulation of transcription induced by oxidative stress utilizes the same epigenetic solutions as those employed in the heat shock response. We also monitored HSP12 induction by 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 to 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 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 of its HAT activity.