Snord116-dependent diurnal rhythm of DNA methylation in mouse cortex

被引：52

作者：

Coulson, Rochelle L. ^{[1
]}

Yasui, Dag H. ^{[1
]}

Dunaway, Keith W. ^{[1
]}

Laufer, Benjamin I. ^{[1
]}

Ciernia, Annie Vogel ^{[1
]}

Zhu, Yihui ^{[1
]}

Mordaunt, Charles E. ^{[1
]}

Totah, Theresa S. ^{[1
]}

LaSalle, Janine M. ^{[1
]}

机构：

[1] Univ Calif Davis, MIND Inst, Genome Ctr, Med Microbiol & Immunol, Davis, CA 95616 USA

来源：

NATURE COMMUNICATIONS | 2018年 / 9卷

基金：

美国国家卫生研究院;

关键词：

PRADER-WILLI-SYNDROME; MATERNAL UNIPARENTAL DISOMY; DLK1-DIO3 IMPRINTED DOMAIN; ANGELMAN-SYNDROME; SLEEP; GENE; EXPRESSION; CHROMATIN; OSCILLATIONS; DISORDERS;

D O I：

10.1038/s41467-018-03676-0

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：11

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