4.7 Article

Developmental regulation of an organelle tether coordinates mitochondrial remodeling in meiosis

期刊

JOURNAL OF CELL BIOLOGY
卷 218, 期 2, 页码 559-579

出版社

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201807097

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资金

  1. Pew Charitable Trusts [00027344]
  2. Damon Runyon Cancer Research Foundation [35-15]
  3. National Institutes of Health [DP2 AG055946-01]
  4. Glenn Foundation for Medical Research
  5. National Science Foundation Graduate Research Fellowship [DGE 1752814, DGE 1106400]
  6. National Institutes of Health Traineeship [T32 GM007127]
  7. National Institutes of Health S10 Instrumentation Grant [S10RR025622]

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Cellular differentiation involves remodeling cellular architecture to transform one cell type to another. By investigating mitochondrial dynamics during meiotic differentiation in budding yeast, we sought to understand how organelle morphogenesis is developmentally controlled in a system where regulators of differentiation and organelle architecture are known, but the interface between them remains unexplored. We analyzed the regulation of mitochondrial detachment from the cell cortex, a known meiotic alteration to mitochondrial morphology. We found that mitochondrial detachment is enabled by the programmed destruction of the mitochondria-endoplasmic reticulum-cortex anchor (MECA), an organelle tether that bridges mitochondria and the plasma membrane. MECA regulation is governed by a meiotic transcription factor, Ndt80, which promotes the activation of a conserved kinase, Ime2. We further present evidence for Ime2-dependent phosphorylation and degradation of MECA in a temporally controlled manner. Our study defines a key mechanism that coordinates mitochondrial morphogenesis with the landmark events of meiosis and demonstrates that cells can developmentally regulate tethering to induce organelle remodeling.

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