PLX283148

GSE95602: HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntingtons disease

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

The heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntingtons disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. SOURCE: David Housman (dhousman@mit.edu) - 76-553 MIT