Document Type

Article

Language

eng

Format of Original

11 p.

Publication Date

1-18-2017

Publisher

Elsevier (Cell Press)

Source Publication

Neuron

Source ISSN

0896-6273

Original Item ID

DOI: 10.1016/j.neuron.2016.12.022

Abstract

A circadian clock governs most aspects of mammalian behavior. Although its properties are in part genetically determined, altered light-dark environment can change circadian period length through a mechanism requiring de novo DNA methylation. We show here that this mechanism is mediated not via cell-autonomous clock properties, but rather through altered networking within the suprachiasmatic nuclei (SCN), the circadian “master clock,” which is DNA methylated in region-specific manner. DNA methylation is necessary to temporally reorganize circadian phasing among SCN neurons, which in turn changes the period length of the network as a whole. Interruption of neural communication by inhibiting neuronal firing or by physical cutting suppresses both SCN reorganization and period changes. Mathematical modeling suggests, and experiments confirm, that this SCN reorganization depends upon GABAergic signaling. Our results therefore show that basic circadian clock properties are governed by dynamic interactions among SCN neurons, with neuroadaptations in network function driven by the environment.

Comments

Accepted version. Neuron, Vol. 93, No. 2 (January 18, 2017): 441-450. DOI. © 2016 Elsevier Inc. Used with permission.

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