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Autophagy-regulated mitochondrial inheritance controls early CD8+ T cell fate commitment.

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Autophagy controls how mitochondria are passed down in CD8+ T cells. Autophagy-deficient cells inherit old mitochondria symmetrically, impacting cell fate and memory potential.

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Area of Science:

  • Immunology
  • Cell Biology
  • Aging Research

Background:

  • T cell immunity declines with age.
  • This decline is linked to reduced autophagy and asymmetric cell division.
  • Mitochondrial quality control is crucial for T cell function.

Purpose of the Study:

  • To investigate the role of autophagy in mitochondrial inheritance in CD8+ T cells.
  • To understand how mitochondrial inheritance impacts T cell fate and function.
  • To explore the metabolic consequences of asymmetric mitochondrial division.

Main Methods:

  • Utilized a mouse model for sequential mitochondrial tagging in mother and daughter cells.
  • Compared autophagy-deficient and autophagy-competent CD8+ T cells.
  • Performed multiomics analyses to assess metabolic programs.

Main Results:

  • Autophagy-deficient T cells showed symmetric inheritance of old mitochondria.
  • Autophagy-competent cells exhibited asymmetric mitochondrial partitioning.
  • Daughter cells retaining old mitochondria had reduced memory potential.
  • Daughter cells with high mitochondrial turnover were long-lived and expanded upon antigen challenge.
  • One-carbon metabolism was activated in cells retaining premitotic mitochondria.

Conclusions:

  • Autophagy is essential for regulating mitochondrial inheritance and T cell fate.
  • Asymmetric mitochondrial division establishes distinct daughter cell populations with differential function.
  • Metabolic reprogramming, including one-carbon metabolism, drives early T cell fate divergence.
  • Findings provide insights into T cell diversity and potential strategies for immune modulation.