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Chromatin remodelling linked with heat acclimation memory suggests epigenetic programming
Author(s) -
Tetievsky Anna,
Horowitz Michal
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.629.7
Subject(s) - chromatin immunoprecipitation , epigenetics , histone , chromatin , histone h4 , acetylation , histone h3 , hsp70 , chromatin remodeling , microbiology and biotechnology , chromatin structure remodeling (rsc) complex , hsf1 , biology , heat shock protein , heat shock , chemistry , promoter , gene expression , gene , genetics
Re‐induction of heat acclimation (AC) after its loss occurs markedly faster than in the initial AC session. We demonstrated that the underlying mechanisms involve continuous upregulation of cytoprotective and chromatin remodeler gene transcripts during deacclimation despite a return of the physiological AC phenotype to pre‐AC. Here we tested the hypothesis that faster re‐AC implicates 'molecular memory' linked to epigenetic modifications. Using our AC(30d)‐DeAC(30d)‐ReAC(2d) R.norvegicus model, histones acetylation (H4, H3) and phosphorylation (H3‐Ser10) at the regions of the heat shock response element (HSE) in HSP70 and HSP90 promoters were measured using Chromatin immunoprecipitation (ChIP). Non‐AC and AC for 2d served as controls. To assess accessibility to the HSE, HSF1‐ChIP at the region of the HSP70 promoter and hsp70 mRNA kinetics following heat stress (HS) were conducted. ChIP analyses provided substantial evidence of chromatin remodelling via histone H4 but not H3 acetylation during AC, DeAC and ReAC. The accessibility of the HSE to HSF1 was validated by its elevated binding in the HSP70 promoter region and by the demonstration of acclimatory mRNA kinetics posts HS in the AC, DeAC and ReAC groups. In conclusion, we provide evidence that long term acclimation induces long standing chromatin remodelling of H4, and so, activates epigenetic mechanisms.