GSBS Student Publications

Student Author(s)

Ania Busza; Jinli Ling

GSBS Program

Neuroscience

UMMS Affiliation

Department of Neurobiology; Emery Lab; Graduate School of Biomedical Sciences, MD/PhD Program; Graduate School of Biomedical Sciences, Neuroscience Program

Date

11-19-2015

Document Type

Article

Disciplines

Molecular and Cellular Neuroscience

Abstract

Circadian clocks integrate light and temperature input to remain synchronized with the day/night cycle. Although light input to the clock is well studied, the molecular mechanisms by which circadian clocks respond to temperature remain poorly understood. We found that temperature phase shifts Drosophila circadian clocks through degradation of the pacemaker protein TIM. This degradation is mechanistically distinct from photic CRY-dependent TIM degradation. Thermal TIM degradation is triggered by cytosolic calcium increase and CALMODULIN binding to TIM and is mediated by the atypical calpain protease SOL. This thermal input pathway and CRY-dependent light input thus converge on TIM, providing a molecular mechanism for the integration of circadian light and temperature inputs. Mammals use body temperature cycles to keep peripheral clocks synchronized with their brain pacemaker. Interestingly, downregulating the mammalian SOL homolog SOLH blocks thermal mPER2 degradation and phase shifts. Thus, we propose that circadian thermosensation in insects and mammals share common principles.

Rights and Permissions

Citation: Cell. 2015 Nov 19;163(5):1214-24. doi: 10.1016/j.cell.2015.10.031. Link to article on publisher's site

DOI of Published Version

10.1016/j.cell.2015.10.031

Comments

Open Access funded by Medical Research Council. Under a Creative Commons license, http://creativecommons.org/licenses/by/4.0/.

Related Resources

Link to Article in PubMed

Journal Title

Cell

PubMed ID

26590423

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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