Activation of the retroviral budding factor ALIX.

نویسندگان

  • Qianting Zhai
  • Michael B Landesman
  • Hyo-Young Chung
  • Adam Dierkers
  • Cy M Jeffries
  • Jill Trewhella
  • Christopher P Hill
  • Wesley I Sundquist
چکیده

The cellular ALIX protein functions within the ESCRT pathway to facilitate intralumenal endosomal vesicle formation, the abscission stage of cytokinesis, and enveloped virus budding. Here, we report that the C-terminal proline-rich region (PRR) of ALIX folds back against the upstream domains and auto-inhibits V domain binding to viral late domains. Mutations designed to destabilize the closed conformation of the V domain opened the V domain, increased ALIX membrane association, and enhanced virus budding. These observations support a model in which ALIX activation requires dissociation of the autoinhibitory PRR and opening of the V domain arms.

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عنوان ژورنال:
  • Journal of virology

دوره 85 17  شماره 

صفحات  -

تاریخ انتشار 2011