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Lamin A safeguards the m6 A methylase METTL14 nuclear speckle reservoir to prevent cellular senescence.
Zhang, Jie; Ao, Ying; Zhang, Zhen; Mo, Yanzhen; Peng, Linyuan; Jiang, Yue; Wang, Zimei; Liu, Baohua.
Affiliation
  • Zhang J; Shenzhen Key Laboratory for Systemic Aging and Intervention, National Engineering Research Center for Biotechnology (Shenzhen), Shenzhen University, Shenzhen, China.
  • Ao Y; Department of Biochemistry & Molecular Biology, Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, School of Basic Medical Sciences, Shenzhen University, Shenzhen, China.
  • Zhang Z; Shenzhen University-Friedrich Schiller Universität Jena Joint PhD Program, Friedrich Schiller Universität, Jena, Germany.
  • Mo Y; Shenzhen Key Laboratory for Systemic Aging and Intervention, National Engineering Research Center for Biotechnology (Shenzhen), Shenzhen University, Shenzhen, China.
  • Peng L; Department of Biochemistry & Molecular Biology, Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, School of Basic Medical Sciences, Shenzhen University, Shenzhen, China.
  • Jiang Y; Shenzhen Key Laboratory for Systemic Aging and Intervention, National Engineering Research Center for Biotechnology (Shenzhen), Shenzhen University, Shenzhen, China.
  • Wang Z; Department of Biochemistry & Molecular Biology, Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, School of Basic Medical Sciences, Shenzhen University, Shenzhen, China.
  • Liu B; Shenzhen University-Friedrich Schiller Universität Jena Joint PhD Program, Friedrich Schiller Universität, Jena, Germany.
Aging Cell ; 19(10): e13215, 2020 10.
Article in En | MEDLINE | ID: mdl-32813328
Mutations in LMNA gene are frequently identified in patients suffering from a genetic disorder known as Hutchison-Gilford progeria syndrome (HGPS), providing an ideal model for the understanding of the mechanisms of aging. Lamin A, encoded by LMNA, is an essential component of the subnuclear domain-nuclear speckles; however, the functional significance in aging is unclear. Here, we show that Lamin A interacts with the m6 A methyltransferases, METTL3 and METTL14 in nuclear speckles. Lamin A deficiency compromises the nuclear speckle METTL3/14 reservoir and renders these methylases susceptible to proteasome-mediated degradation. Moreover, METTL3/14 levels progressively decline in cells undergoing replicative senescence. Overexpression of METTL14 attenuates both replicative senescence and premature senescence. The data reveal an essential role for Lamin A in safeguarding the nuclear speckle reservoir of the m6 A methylase METTL14 to antagonize cellular senescence.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Lamin Type A / Methyltransferases Limits: Humans Language: En Journal: Aging Cell Year: 2020 Document type: Article Affiliation country: China Country of publication: Reino Unido

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Lamin Type A / Methyltransferases Limits: Humans Language: En Journal: Aging Cell Year: 2020 Document type: Article Affiliation country: China Country of publication: Reino Unido