miR-132/212 Modulates Seasonal Adaptation and Dendritic Morphology of the Central Circadian Clock

Publication date: 18 April 2017
Source:Cell Reports, Volume 19, Issue 3
Author(s): Lucia Mendoza-Viveros, Cheng-Kang Chiang, Jonathan L.K. Ong, Sara Hegazi, Arthur H. Cheng, Pascale Bouchard-Cannon, Michael Fana, Christopher Lowden, Peng Zhang, Béatrice Bothorel, Matthew G. Michniewicz, Stephen T. Magill, Melissa M. Holmes, Richard H. Goodman, Valérie Simonneaux, Daniel Figeys, Hai-Ying M. Cheng
The central circadian pacemaker, the suprachiasmatic nucleus (SCN), encodes day length information by mechanisms that are not well understood. Here, we report that genetic ablation of miR-132/212 alters entrainment to different day lengths and non-24 hr day-night cycles, as well as photoperiodic regulation of Period2 expression in the SCN. SCN neurons from miR-132/212-deficient mice have significantly reduced dendritic spine density, along with altered methyl CpG-binding protein (MeCP2) rhythms. In Syrian hamsters, a model seasonal rodent, day length regulates spine density on SCN neurons in a melatonin-independent manner, as well as expression of miR-132, miR-212, and their direct target, MeCP2. Genetic disruption of Mecp2 fully restores the level of dendritic spines of miR-132/212-deficient SCN neurons. Our results reveal that, by regulating the dendritic structure of SCN neurons through a MeCP2-dependent mechanism, miR-132/212 affects the capacity of the SCN to encode seasonal time.

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Teaser

Seasonal adaptation is believed to require plasticity in the SCN, although the mechanisms are unclear. Mendoza-Viveros et al. report that miR-132/212 modulates dendritic protrusion density and photoperiodic adaptation in mice and hamsters, by regulating the expression of MeCP2, and downstream BDNF and mTOR signaling.


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