Heat acclimation memory: Does the de-acclimated transcriptome reveal epigenetic processes of transcriptional regulation?

Heat acclimation (AC) allows its faster re-induction following its decline. Constitutively preserved euchromatin state in hsp70 promoter during acclimation decline/regain pushed forward the hypothesis that acclimation decline is a period of “dormant memory” involving molecular program including epigenetic controlled transcriptional regulation leading to heat acclimation mediated cytoprotective memory. We used microarray to uncover hallmark pathways in the induction of heat-acclimation-mediated memory, focusing on markers of epigenetic processes. Rats subjected to heat acclimation, deacclimation, reacclimation and untreated controls were used. We showed here that (i) AC2d provides the molecular switch for acclimation (ii) AC30 heart demonstrates qualitative adaptations (iii) specific molecular program encompassing up/down regulated gene during DeAC, of which epigenetic markers such as class A histones, chromatin modifiers and microRNA suggest epigenetic transcriptional regulation linked to acclimation memory (iv) constitutive upregulation of MAPK P38 module and targets as well as jak/stat and AKT associated pathways during DeAC imply its major role in this process. Noteworthy are players such as poly-(ADP-ribose)polymerase-1 (PARP1) and linker histones (histones H1 cluster in this process).