Regulation of mitochondrial plasticity by the i-AAA protease YME1L

Yohsuke Ohba, Thomas MacVicar, Thomas Langer

研究成果: Review article査読

16 被引用数 (Scopus)

抄録

Mitochondria are multifaceted metabolic organelles and adapt dynamically to various developmental transitions and environmental challenges. The metabolic flexibility of mitochondria is provided by alterations in the mitochondrial proteome and is tightly coupled to changes in the shape of mitochondria. Mitochondrial proteases are emerging as important posttranslational regulators of mitochondrial plasticity. The i-AAA protease YME1L, an ATP-dependent proteolytic complex in the mitochondrial inner membrane, coordinates mitochondrial biogenesis and dynamics with the metabolic output of mitochondria. mTORC1-dependent lipid signaling drives proteolytic rewiring of mitochondria by YME1L. While the tissue-specific loss of YME1L in mice is associated with heart failure, disturbed eye development, and axonal degeneration in the spinal cord, YME1L activity supports growth of pancreatic ductal adenocarcinoma cells. YME1L thus represents a key regulatory protease determining mitochondrial plasticity and metabolic reprogramming and is emerging as a promising therapeutic target.

本文言語English
ページ(範囲)877-890
ページ数14
ジャーナルBiological Chemistry
401
6-7
DOI
出版ステータスPublished - 2020 5月 26
外部発表はい

ASJC Scopus subject areas

  • 生化学
  • 分子生物学
  • 臨床生化学

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