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Related Experiment Videos

A Metabolic Function for Phospholipid and Histone Methylation.

Cunqi Ye1, Benjamin M Sutter1, Yun Wang1

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

Molecular Cell
|April 4, 2017
PubMed
Summary
This summary is machine-generated.

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Phospholipid methylation, specifically of phosphatidylethanolamine (PE), is a major consumer of S-adenosylmethionine (SAM). Disrupting this process leads to metabolic dysfunction and cellular stress.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Pathways

Background:

  • S-adenosylmethionine (SAM) is the primary methyl donor for crucial biological methylation reactions.
  • Phospholipid methylation, particularly of phosphatidylethanolamine (PE), has not been recognized as a significant consumer of SAM.
  • S-adenosylhomocysteine (SAH) is a byproduct of SAM-dependent methylation and an inhibitor of methyltransferases.

Purpose of the Study:

  • To investigate the role of phosphatidylethanolamine (PE) methylation in S-adenosylmethionine (SAM) metabolism.
  • To understand the consequences of impaired PE methylation on cellular metabolic homeostasis.
  • To elucidate the link between phospholipid methylation, histone modifications, and cellular stress responses.

Main Methods:

  • Analysis of gene expression for phospholipid biosynthesis and S-adenosylhomocysteine (SAH) hydrolysis.
Keywords:
H3K36S-adenosylmethioninecysteineepigeneticsglutathionehistone methylationmethyltransferasephospholipidstranssulfuration

Related Experiment Videos

  • Metabolic flux analysis to track S-adenosylmethionine (SAM) consumption and turnover.
  • Assessment of histone methylation patterns and cellular sensitivity to oxidative stress in cells with altered PE methylation.

    • Main Results:

    • Phosphatidylethanolamine (PE) methylation is identified as a major pathway for S-adenosylmethionine (SAM) consumption.
    • The methylation of PE supports SAM turnover for cysteine and glutathione synthesis via transsulfuration.
    • Cells lacking PE methylation exhibit S-adenosylmethionine (SAM) accumulation, leading to histone and PP2A hypermethylation, cysteine dependency, and oxidative stress sensitivity.

    Conclusions:

    • Phospholipid methylation plays a critical, previously unrecognized role in regulating S-adenosylmethionine (SAM) metabolism.
    • Impaired PE methylation disrupts cellular SAM homeostasis, impacting histone methylation and increasing susceptibility to oxidative stress.
    • This study reveals a fundamental metabolic function of phospholipid and histone methylation essential for cell survival.