Dataset Information

Multitissue Circadian Proteome Atlas of WT and Per1^-/-/Per2^-/- Mice.

ABSTRACT: The molecular basis of circadian rhythm, driven by core clock genes such as Per1/2, has been investigated on the transcriptome level, but not comprehensively on the proteome level. Here we quantified over 11,000 proteins expressed in eight types of tissues over 46 h with an interval of 2 h, using WT and Per1/Per2 double knockout mouse models. The multitissue circadian proteome landscape of WT mice shows tissue-specific patterns and reflects circadian anticipatory phenomena, which are less obvious on the transcript level. In most peripheral tissues of double knockout mice, reduced protein cyclers are identified when compared with those in WT mice. In addition, PER1/2 contributes to controlling the anticipation of the circadian rhythm, modulating tissue-specific cyclers as well as key pathways including nucleotide excision repair. Severe intertissue temporal dissonance of circadian proteome has been observed in the absence of Per1 and Per2. The γ-aminobutyric acid might modulate some of these temporally correlated cyclers in WT mice. Our study deepens our understanding of rhythmic proteins across multiple tissues and provides valuable insights into chronochemotherapy. The data are accessible at https://prot-rhythm.prottalks.com/.

SUBMITTER: Qian L

PROVIDER: S-EPMC10750102 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Multitissue Circadian Proteome Atlas of WT and Per1<sup>-/-</sup>/Per2<sup>-/-</sup> Mice.

Qian Liujia L Gu Yue Y Zhai Qiaocheng Q Xue Zhangzhi Z Liu Youqi Y Li Sainan S Zeng Yizhun Y Sun Rui R Zhang Qiushi Q Cai Xue X Ge Weigang W Dong Zhen Z Gao Huanhuan H Zhou Yan Y Zhu Yi Y Xu Ying Y Guo Tiannan T

Molecular & cellular proteomics : MCP 20231107 12

The molecular basis of circadian rhythm, driven by core clock genes such as Per1/2, has been investigated on the transcriptome level, but not comprehensively on the proteome level. Here we quantified over 11,000 proteins expressed in eight types of tissues over 46 h with an interval of 2 h, using WT and Per1/Per2 double knockout mouse models. The multitissue circadian proteome landscape of WT mice shows tissue-specific patterns and reflects circadian anticipatory phenomena, which are less obviou ...[more]

PMID: 37940002

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Project description:Human and animal studies demonstrate that short sleep or poor sleep quality, e.g. in night shift workers, promote the development of obesity and diabetes. Effects of sleep disruption on glucose homeostasis and liver physiology are well documented. However, changes in adipokine levels after sleep disruption suggest that adipocytes might be another important peripheral target of sleep. Circadian clocks regulate metabolic homeostasis and clock disruption can result in obesity and the metabolic syndrome. The finding that sleep and clock disruption have very similar metabolic effects prompted us to ask whether the circadian clock machinery may mediate the metabolic consequences of sleep disruption. To test this we analyzed energy homeostasis and adipocyte transcriptome regulation in a mouse model of shift work, in which we prevented mice from sleeping during the first six hours of their normal inactive phase for five consecutive days (timed sleep restriction--TSR). We compared the effects of TSR between wild-type and Per1/2 double mutant mice with the prediction that the absence of a circadian clock in Per1/2 mutants would result in a blunted metabolic response to TSR. In wild-types, TSR induces significant transcriptional reprogramming of white adipose tissue, suggestive of increased lipogenesis, together with increased secretion of the adipokine leptin and increased food intake, hallmarks of obesity and associated leptin resistance. Some of these changes persist for at least one week after the end of TSR, indicating that even short episodes of sleep disruption can induce prolonged physiological impairments. In contrast, Per1/2 deficient mice show blunted effects of TSR on food intake, leptin levels and adipose transcription. We conclude that the absence of a functional clock in Per1/2 double mutants protects these mice from TSR-induced metabolic reprogramming, suggesting a role of the circadian timing system in regulating the physiological effects of sleep disruption.

Dataset Information

Multitissue Circadian Proteome Atlas of WT and Per1^-/-/Per2^-/- Mice.

Publications

Multitissue Circadian Proteome Atlas of WT and Per1<sup>-/-</sup>/Per2<sup>-/-</sup> Mice.

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Dataset Information

Multitissue Circadian Proteome Atlas of WT and Per1-/-/Per2-/- Mice.

Publications

Multitissue Circadian Proteome Atlas of WT and Per1<sup>-/-</sup>/Per2<sup>-/-</sup> Mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Multitissue Circadian Proteome Atlas of WT and Per1^-/-/Per2^-/- Mice.