Snord116-dependent diurnal rhythm of DNA methylation in mouse cortex

Rochelle L. Coulson, Dag H. Yasui, Keith W. Dunaway, Benjamin I. Laufer, Annie Vogel Ciernia, Yihui Zhu, Charles E. Mordaunt, Theresa S. Totah and Janine M. LaSalle ()
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Rochelle L. Coulson: University of California
Dag H. Yasui: University of California
Keith W. Dunaway: University of California
Benjamin I. Laufer: University of California
Annie Vogel Ciernia: University of California
Yihui Zhu: University of California
Charles E. Mordaunt: University of California
Theresa S. Totah: University of California
Janine M. LaSalle: University of California

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract Rhythmic oscillations of physiological processes depend on integrating the circadian clock and diurnal environment. DNA methylation is epigenetically responsive to daily rhythms, as a subset of CpG dinucleotides in brain exhibit diurnal rhythmic methylation. Here, we show a major genetic effect on rhythmic methylation in a mouse Snord116 deletion model of the imprinted disorder Prader–Willi syndrome (PWS). More than 23,000 diurnally rhythmic CpGs are identified in wild-type cortex, with nearly all lost or phase-shifted in PWS. Circadian dysregulation of a second imprinted Snord cluster at the Temple/Kagami-Ogata syndrome locus is observed at the level of methylation, transcription, and chromatin, providing mechanistic evidence of cross-talk. Genes identified by diurnal epigenetic changes in PWS mice overlapped rhythmic and PWS-specific genes in human brain and are enriched for PWS-relevant phenotypes and pathways. These results support the proposed evolutionary relationship between imprinting and sleep, and suggest possible chronotherapy in the treatment of PWS and related disorders.

Date: 2018
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DOI: 10.1038/s41467-018-03676-0

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