| Literature DB >> 32694864 |
Zuojun Liu1,2,3, Minxian Qian1,2,3, Xiaolong Tang1,2,3, Wenjing Hu2,4, Shimin Sun2,4, Guo Li5, Shuju Zhang2,3, Fanbiao Meng2,3, Xinyue Cao2,3, Jie Sun1,2,3, Cheng Xu1,2,3, Bing Tan1,2,3, Qiuxiang Pang4, Bosheng Zhao4, Zimei Wang1,3, Youfei Guan6, Xiongzhong Ruan7,8, Baohua Liu9,10,11.
Abstract
The central pacemaker in the hypothalamic suprachiasmatic nucleus (SCN) synchronizes peripheral oscillators to coordinate physiological and behavioural activities throughout the body. How circadian phase coherence between the SCN and the periphery is controlled is not well understood. Here, we identify hepatic SIRT7 as an early responsive element to light that ensures circadian phase coherence in the mouse liver. The SCN-driven body temperature (BT) oscillation induces rhythmic expression of HSP70, which promotes SIRT7 ubiquitination and proteasomal degradation. Acute temperature challenge dampens the BT oscillation and causes an advanced liver circadian phase. Further, hepatic SIRT7 deacetylates CRY1, promotes its FBXL3-mediated degradation and regulates the hepatic clock and glucose homeostasis. Loss of Sirt7 in mice leads to an advanced liver circadian phase and rapid entrainment of the hepatic clock upon daytime-restricted feeding. These data identify a BT-HSP70-SIRT7-CRY1 axis that couples the mouse hepatic clock to the central pacemaker and ensures circadian phase coherence and glucose homeostasis.Entities:
Mesh：
Substances：
Year: 2019 PMID： 32694864 DOI： 10.1038/s42255-019-0136-6
Source DB: PubMed Journal: Nat Metab ISSN： 2522-5812