| Literature DB >> 32268083 |
Mayumi Hirayama1, Fan-Yan Wei2, Takeshi Chujo3, Shinya Oki4, Maya Yakita1, Daiki Kobayashi5, Norie Araki5, Nozomu Takahashi6, Ryoji Yoshida6, Hideki Nakayama6, Kazuhito Tomizawa7.
Abstract
N6-Methyladenosine (m6A) modification is the major chemical modification in mRNA that controls fundamental biological processes, including cell proliferation. Herein, we demonstrate that fat mass and obesity-associated (FTO) demethylates m6A modification of cyclin D1, the key regulator for G1 phase progression and controls cell proliferation in vitro and in vivo. FTO depletion upregulates cyclin D1 m6A modification, which in turn accelerates the degradation of cyclin D1 mRNA, leading to the impairment of G1 progression. m6A modification of cyclin D1 oscillates in a cell-cycle-dependent manner; m6A levels are suppressed during the G1 phase and enhanced during other phases. Low m6A levels during G1 are associated with the nuclear translocation of FTO from the cytosol. Furthermore, nucleocytoplasmic shuttling of FTO is regulated by casein kinase II-mediated phosphorylation of FTO. Our results highlight the role of m6A in regulating cyclin D1 mRNA stability and add another layer of complexity to cell-cycle regulation.Entities:
Keywords: FTO; N(6)-methyladenosine; RNA; casein kinase; cell cycle; cyclin D1; modification; phosphorylation
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Year: 2020 PMID: 32268083 DOI: 10.1016/j.celrep.2020.03.028
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423