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The HPV16 E5 oncogene inhibits endocytic trafficking
P Thomsen1, B van Deurs, B Norrild
1Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Denmark.
Oncogene
|January 9, 2001
Summary
Human Papillomavirus type 16 (HPV16) E5 protein disrupts endocytic trafficking. HPV16 E5 perturbs the movement of cellular components to late endocytic structures, rather than affecting their acidification.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- The E5 protein of Human Papillomavirus type 16 (HPV16) is a small hydrophobic protein.
- HPV16 E5 is known to interact with the V-H+-ATPase.
- Previous studies suggested HPV16 E5 binding interferes with the acidification of late endocytic structures.
Purpose of the Study:
- To investigate the effects of HPV16 E5 on endocytic trafficking and acidification in living cells.
- To determine whether HPV16 E5 inhibits acidification or perturbs the trafficking of endocytic markers.
Main Methods:
- Utilized video microscopy, ratio imaging, and confocal microscopy on living C127 fibroblasts.
- Employed various endocytic markers, including pH-sensitive probes (DM-NERF-dextran) and fluorescent tracers (TransFluoSpheres, TRITC-concanavalin A).
- Assessed colocalization with acidic late endocytic structures (LysoTracker Red) and Rab7-labeled structures.
Main Results:
- In cells expressing HPV16 E5, endocytic markers did not colocalize with LysoTracker Red or Rab7.
- Late endocytic structures that accumulate LysoTracker Red remained present in E5-expressing cells.
- The observed effects were specific to E5 expression.
Conclusions:
- Human Papillomavirus type 16 E5 protein perturbs the trafficking of molecules from early to late endocytic compartments.
- HPV16 E5 does not inhibit the acidification of late endocytic structures.
- The mechanism of HPV16 E5 involves interference with endocytic pathway progression.