Exposure to temperatures exceeding the normal optimum levels, or heat stress (HS), constitutes an environmental disruption for plants, resulting in severe growth and development retardation. Here we show that loss of function of the Arabidopsis histone acetyltransferase GCN5 results in serious defects in terms of thermotolerance, and considerably impairs the transcriptional activation of HS-responsive genes. Notably, expression of several key regulators such as the HS transcription factorsHSFA2andHSFA3,Multiprotein Bridging Factor 1c(MBF1c) andUV-HYPERSENSITIVE 6(UVH6) is down-regulated in thegcn5mutant under HS compared with the wild-type. Chromatin immunoprecipitation (ChIP) assays indicated that GCN5 protein is enriched at the promoter regions ofHSFA3andUVH6genes, but not inHSFA2andMBF1c, and that GCN5 facilitates H3K9 and H3K14 acetylation, which are associated withHSFA3andUVH6activation under HS. Moreover, constitutive expression ofUVH6in thegcn5mutant partially restores heat tolerance. Taken together, our data indicate that GCN5 plays a key role in the preservation of thermotolerance via versatile regulation in Arabidopsis. In addition, expression of the wheatTaGCN5gene re-establishes heat tolerance in Arabidopsisgcn5mutant plants, suggesting that GCN5-mediated thermotolerance may be conserved between Arabidopsis and wheat.Significance Statement
Histone modifications are major epigenetic mechanisms that regulate gene expression and plant growth and development. Here, we demonstrate that a histone acetyltransferase mutant acquires heat-sensitive phenotypes due to the impaired transcriptional activation of heat stress-responsive genes.