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Methionine inhibits autophagy and promotes growth by inducing the SAM-responsive methylation of PP2A

Benjamin M Sutter1, Xi Wu, Sunil Laxman

  • 1Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.

Cell
|July 23, 2013
PubMed

Insights

Methionine inhibits yeast autophagy by boosting S-adenosylmethionine (SAM) synthesis. SAM activates methyltransferase Ppm1p, which modifies PP2A to regulate cell growth and autophagy based on amino acid availability.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Autophagy is cellular self-digestion, typically triggered by starvation.
  • Yeast can initiate autophagy even without nitrogen starvation when switching media.
  • Understanding triggers for non-nitrogen-starvation (NNS)-induced autophagy is crucial for cellular regulation.

Purpose of the Study:

  • To investigate the role of methionine in regulating non-nitrogen-starvation (NNS)-induced autophagy in yeast.
  • To elucidate the molecular mechanism by which methionine influences autophagy.
  • To identify key proteins and pathways involved in sensing amino acid availability for autophagy control.

Main Methods:

  • Yeast cell culture under varying media conditions.
  • Measurement of autophagy markers.
  • Analysis of S-adenosylmethionine (SAM) levels.
  • Enzyme activity assays for Ppm1p and PP2A.
  • Phosphorylation analysis of Npr2p.

Main Results:

  • Methionine was identified as sufficient to inhibit NNS-induced autophagy.
  • Methionine increases S-adenosylmethionine (SAM) levels, a key methyl donor.
  • SAM-dependent methylation of PP2A by Ppm1p was observed.
  • Methylated PP2A dephosphorylates Npr2p, regulating autophagy and growth.

Conclusions:

  • Methionine and SAM levels act as critical sensors of amino acid availability.
  • The methylation of PP2A by Ppm1p is a key mechanism linking SAM levels to NNS autophagy.
  • This pathway reciprocally regulates yeast cell growth and autophagy in response to nutrient status.

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