Cold-induced chromatin compaction and nuclear retention of clock mRNAs resets the circadian rhythm.
Harry FischlDavid McManusRoel OldenkampLothar SchermellehJane MellorAarti JagannathAndré Martin FurgerPublished in: The EMBO journal (2020)
Cooling patients to sub-physiological temperatures is an integral part of modern medicine. We show that cold exposure induces temperature-specific changes to the higher-order chromatin and gene expression profiles of human cells. These changes are particularly dramatic at 18°C, a temperature synonymous with that experienced by patients undergoing controlled deep hypothermia during surgery. Cells exposed to 18°C exhibit largely nuclear-restricted transcriptome changes. These include the nuclear accumulation of mRNAs encoding components of the negative limbs of the core circadian clock, most notably REV-ERBα. This response is accompanied by compaction of higher-order chromatin and hindrance of mRNPs from engaging nuclear pores. Rewarming reverses chromatin compaction and releases the transcripts into the cytoplasm, triggering a pulse of negative limb gene proteins that reset the circadian clock. We show that cold-induced upregulation of REV-ERBα is sufficient to trigger this reset. Our findings uncover principles of the cellular cold response that must be considered for current and future applications involving therapeutic deep hypothermia.
Keyphrases
- genome wide
- gene expression
- dna damage
- transcription factor
- dna methylation
- patients undergoing
- end stage renal disease
- copy number
- high glucose
- cardiac arrest
- diabetic rats
- induced apoptosis
- newly diagnosed
- ejection fraction
- minimally invasive
- chronic kidney disease
- peritoneal dialysis
- oxidative stress
- atrial fibrillation
- brain injury
- genome wide identification
- drug induced
- signaling pathway
- cell proliferation
- rna seq
- coronary artery disease
- cell cycle arrest
- heart rate
- current status
- prognostic factors
- patient reported outcomes
- cell death
- patient reported
- surgical site infection