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Nef-mediated clathrin-coated pit formation

M Foti1, A Mangasarian, V Piguet

  • 1Department of Morphology, Centre Médical Universitaire, University of Geneva, Switzerland.

The Journal of Cell Biology
|October 6, 1997
PubMed
Summary
This summary is machine-generated.

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Human immunodeficiency virus (HIV) Nef protein accelerates CD4 receptor endocytosis by promoting clathrin-coated pit (CCP) assembly. This process requires the CD4 cytoplasmic tail, suggesting receptors can initiate CCP formation.

Area of Science:

  • Cell biology
  • Virology
  • Molecular mechanisms of endocytosis

Background:

  • The precise mechanisms governing clathrin-coated pit (CCP) nucleation and receptor incorporation during endocytosis remain unclear.
  • It is debated whether receptor tails initiate CCP assembly or if receptors enter pre-existing CCPs.

Purpose of the Study:

  • To investigate the role of Nef, a protein from human and simian immunodeficiency viruses (HIV and SIV), in accelerating the endocytosis of CD4, the primary receptor for these viruses.
  • To elucidate the molecular mechanisms by which Nef influences CD4 internalization and CCP formation.

Main Methods:

  • Analysis of CD4-CCP association and CCP dynamics at the plasma membrane in the presence of Nef.
  • Investigation of the necessity of the CD4 cytoplasmic tail and its dileucine motif for Nef-mediated CCP induction.

Related Experiment Videos

  • Experiments assessing Nef's ability to induce CCP formation when directly anchored to the plasma membrane.

    • Main Results:

    • Nef enhances CD4 internalization by increasing CD4's association with CCPs.
    • Nef significantly increases the plasma membrane area occupied by clathrin-coated structures, primarily affecting CD4 uptake without impacting transferrin receptor or fluid-phase endocytosis.
    • A functional CD4 cytoplasmic tail with a dileucine motif is essential for Nef to induce CCP formation.
    • Nef can independently promote CCP formation when localized to the cytoplasmic side of the plasma membrane.

    Conclusions:

    • CD4, through the connector molecule Nef, can promote CCP generation.
    • A proposed model suggests Nef bridges CD4's dileucine motif with CCP components (adaptins), initiating CCP nucleation.
    • This study provides evidence that receptors, via specific viral proteins, can actively drive the formation of endocytic machinery.