Mechanisms of PI(4,5)P2 Enrichment in HIV-1 Viral Membranes.


Journal

Journal of molecular biology
ISSN: 1089-8638
Titre abrégé: J Mol Biol
Pays: Netherlands
ID NLM: 2985088R

Informations de publication

Date de publication:
04 09 2020
Historique:
received: 01 06 2020
revised: 12 07 2020
accepted: 26 07 2020
pubmed: 3 8 2020
medline: 10 3 2021
entrez: 3 8 2020
Statut: ppublish

Résumé

Phosphatidylinositol 4,5-bisphosphate (PIP2) is critical for HIV-1 virus assembly. The viral membrane is enriched in PIP2, suggesting that the virus assembles at PIP2-rich microdomains. We showed previously that in model membranes PIP2 can form nanoscopic clusters bridged by multivalent cations. Here, using purified proteins we quantitated the binding of HIV-1 Gag-related proteins to giant unilamellar vesicles containing either clustered or free PIP2. Myristoylated MA strongly preferred binding to clustered PIP2. By contrast, unmyristoylated HIV-1 MA, RSV MA, and a PH domain all preferred to interact with free PIP2. We also found that HIV-1 Gag multimerization promotes PIP2 clustering. Truncated Gag proteins comprising the MA, CA, and SP domains (MACASP) or the MA and CA domains (MACA) induced self-quenching of acyl chain-labeled fluorescent PIP2 in liposomes, implying clustering. However, HIV-1 MA itself did not induce PIP2 clustering. A CA inter-hexamer dimer interface mutation led to a loss of induced PIP2 clustering in MACA, indicating the importance of protein multimerization. Cryo-electron tomography of liposomes with bound MACA showed an amorphous protein layer on the membrane surface. Thus, it appears that while protein-protein interactions are required for PIP2 clustering, formation of a regular lattice is not. Protein-induced PIP2 clustering and multivalent cation-induced PIP2 clustering are additive. Taken together, these results provide the first evidence that HIV-1 Gag can selectively target pre-existing PIP2-enriched domains of the plasma membrane for viral assembly, and that Gag multimerization can further enrich PIP2 at assembly sites. These effects could explain the observed PIP2 enrichment in HIV-1.

Identifiants

pubmed: 32739462
pii: S0022-2836(20)30473-3
doi: 10.1016/j.jmb.2020.07.018
pmc: PMC8262684
mid: NIHMS1717033
pii:
doi:

Substances chimiques

Phosphatidylinositol 4,5-Diphosphate 0
Unilamellar Liposomes 0
gag Gene Products, Human Immunodeficiency Virus 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

5343-5364

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI147890
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI150454
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM105684
Pays : United States

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Yi Wen (Y)

Department of Molecular Biology & Genetics, Cornell University, Ithaca, NY 14853, USA.

Gerald W Feigenson (GW)

Department of Molecular Biology & Genetics, Cornell University, Ithaca, NY 14853, USA.

Volker M Vogt (VM)

Department of Molecular Biology & Genetics, Cornell University, Ithaca, NY 14853, USA.

Robert A Dick (RA)

Department of Molecular Biology & Genetics, Cornell University, Ithaca, NY 14853, USA. Electronic address: rad82@cornell.edu.

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Classifications MeSH