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Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
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Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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The ER synthesizes lipids for building cell membranes and performing cellular functions such as energy storage and signaling. The lipid synthesis machinery embedded in the ER membrane primarily collects all reactants from the cytosol. Following synthesis, the secretory pathway and the ER contact sites distribute these lipids to other cellular organelles. Additionally, the energy-rich triacylglycerides are transported from the ER via lipid droplets.
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Biological membranes show uneven distribution of different types of lipids in the inner and outer layers, resulting in transverse asymmetric membranes. The treatment of the erythrocyte membrane with the enzyme phospholipase confirmed the asymmetric nature of the lipid bilayer. The enzyme hydrolyzes lipids into fatty acids and hydrophilic groups. The phospholipase acts only on the outer layer of the membrane, while the inner layer remains intact. The phospholipase treatment resulted in 80%...
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Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
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Sphingolipid Long-Chain Base Phosphate Degradation Can Be a Rate-Limiting Step in Long-Chain Base Homeostasis.

Benjamin Lambour1, René Glenz1, Carmen Forner1

  • 1Pharmaceutical Biology, Julius-von-Sachs Institute of Biosciences, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.

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High levels of sphingolipids (LCBs) in plants can trigger cell death. This study shows that dihydrosphingosine-1-phosphate lyase 1 (DPL1) helps reduce LCBs, increasing plant resistance to toxins.

Keywords:
LC–MS/MScell deathdihydrosphingosine-1-phosphate lyaselong-chain basemetabolic flux analysisplant sphingolipid metabolismsphingolipid

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Area of Science:

  • Plant Biochemistry
  • Molecular Biology
  • Cell Death Pathways

Background:

  • Sphingolipids, specifically long-chain bases (LCBs), are crucial for plant cell membranes and signaling.
  • Elevated LCB levels are linked to programmed cell death and sensitivity to pathogen toxins, impacting plant survival.
  • Understanding metabolic pathways that regulate LCB levels is key to controlling plant cell fate.

Purpose of the Study:

  • To investigate the metabolic fate of LCBs in Arabidopsis leaves using deuterium-labeled precursors.
  • To identify key enzymatic pathways involved in reducing high LCB levels.
  • To functionally test the role of dihydrosphingosine-1-phosphate lyase 1 (DPL1) in LCB regulation and plant defense.

Main Methods:

  • Application of deuterium-labeled D-erythro-sphinganine-d7 (D7-d18:0) to Arabidopsis leaves.
  • Quantification of labeled LCBs, LCB phosphates (LCB-Ps), and ceramides (Cers) over time.
  • Construction and analysis of a transgenic Arabidopsis line with inducible DPL1 expression.

Main Results:

  • D7-d18:0 was rapidly converted into other LCBs and LCB-Ps, with a significant increase in LCB-P levels.
  • Labeled ceramides, particularly Cer(d18:0/16:0) and Cer(d18:0/24:0), increased over time.
  • Overexpression of DPL1 reduced elevated LCB-P and LCB levels induced by Fumonisin B1, enhancing plant resistance.

Conclusions:

  • LCB-P degradation is a critical pathway for reducing high LCB levels in plants.
  • DPL1 plays a rate-limiting role in the degradation of LCB-Ps, thereby controlling LCB levels.
  • Modulating DPL1 activity offers a potential strategy to enhance plant tolerance to LCB-mediated cell death triggers.