4.8 Article

Multiple phosphorylation events of the mitochondrial membrane protein TTM1 regulate cell death during senescence

期刊

PLANT JOURNAL
卷 108, 期 3, 页码 766-780

出版社

WILEY
DOI: 10.1111/tpj.15470

关键词

abscisic acid; Arabidopsis thaliana; MAP kinase; mitochondria; programmed cell death; senescence; triphosphate tunnel metalloenzyme

资金

  1. Canadian Foundation for Innovation
  2. Ontario Research Fund
  3. Ontario graduate Scholarship

向作者/读者索取更多资源

TTM1 is specifically involved in senescence induced by ABA, and its function and turnover are regulated by multiple MAP kinases, with phosphorylation of Ser437 being essential for its function in senescence. Multiple MAP kinases mark TTM1 for protein turnover by phosphorylating Ser10 and Ser490 as well, preventing uncontrolled cell death. This study reveals a novel link between mitochondria and PCD during senescence-associated cell death.
The role of mitochondria in programmed cell death (PCD) during animal growth and development is well documented, but much less is known for plants. We previously showed that the Arabidopsis thaliana triphosphate tunnel metalloenzyme (TTM) proteins TTM1 and TTM2 are tail-anchored proteins that localize in the mitochondrial outer membrane and participate in PCD during senescence and immunity, respectively. Here, we show that TTM1 is specifically involved in senescence induced by abscisic acid (ABA). Moreover, phosphorylation of TTM1 by multiple mitogen-activated protein (MAP) kinases regulates its function and turnover. A combination of proteomics and in vitro kinase assays revealed three major phosphorylation sites of TTM1 (Ser10, Ser437, and Ser490). Ser437, which is phosphorylated upon perception of senescence cues such as ABA and prolonged darkness, is phosphorylated by the MAP kinases MPK3 and MPK4, and Ser437 phosphorylation is essential for TTM1 function in senescence. These MPKs, together with three additional MAP kinases (MPK1, MPK7, and MPK6), also phosphorylate Ser10 and Ser490, marking TTM1 for protein turnover, which likely prevents uncontrolled cell death. Taken together, our results show that multiple MPKs regulate the function and turnover of the mitochondrial protein TTM1 during senescence-associated cell death, revealing a novel link between mitochondria and PCD.

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