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Depletion-mode MOSFETs represent a unique subset of MOSFET technology, functioning fundamentally differently from their enhancement-mode counterparts. Unlike enhancement MOSFETs, which require a positive gate-source voltage (Vgs) to turn on, depletion-mode MOSFETs are inherently conductive and "normally on" devices.
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Cholesterol depletion activates trafficking-coupled sphingolipid synthesis.

Yeongho Kim1, Jan Parolek1, Christopher G Burd1

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Cell cholesterol depletion increases very-long-chain (VLC) sphingomyelin synthesis by enhancing VLC-ceramide transport from the endoplasmic reticulum to the Golgi. The protein cTAGE5 acts as a sensor for this ceramide export.

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Area of Science:

  • Cell Biology
  • Lipid Metabolism
  • Membrane Trafficking

Background:

  • Homeostatic pathways regulate organelle membrane lipid composition.
  • Mechanistic links between lipid sensing, synthesis, and trafficking remain unclear.
  • Cell cholesterol depletion impacts sphingomyelin synthesis and plasma membrane cholesterol levels.

Purpose of the Study:

  • To elucidate the mechanisms linking cholesterol homeostasis to lipid synthesis and trafficking.
  • To identify the molecular players involved in very-long-chain (VLC) ceramide transport.
  • To investigate the role of cTAGE5 in endoplasmic reticulum (ER)-to-Golgi transport.

Main Methods:

  • Stable isotope metabolic analyses.
  • Lipid trafficking assays.
  • Protein localization and interaction studies (photochemical cross-linking).

Main Results:

  • Acute cholesterol depletion increases VLC-sphingomyelin synthesis in the Golgi.
  • This increase is driven by enhanced coatomer II-dependent VLC-ceramide trafficking from the ER to the Golgi.
  • The integral membrane protein cTAGE5 is essential for ER-to-Golgi ceramide transport.
  • cTAGE5 overexpression leads to ER network herniations and traps ceramide analogs.

Conclusions:

  • cTAGE5 functions as a ceramide sensor at the ER exit site.
  • cTAGE5 regulates the export of VLC-ceramide from the ER.
  • This pathway links cellular cholesterol levels to the synthesis of VLC-sphingomyelin.