Lineage-Specific Viral Hijacking of Non-canonical E3 Ubiquitin Ligase Cofactors in the Evolution of Vif Anti-APOBEC3 Activity

Joshua R. Kane; David J. Stanley; Judd F. Hultquist; Jeffrey R. Johnson; Nicole Mietrach; Jennifer M. Binning; Stefán R. Jónsson; Sarah Barelier; Billy W. Newton; Tasha L. Johnson; Kathleen E. Franks-Skiba; Ming Li; William L. Brown; Hörður I. Gunnarsson; Adalbjorg Adalbjornsdóttir; James S. Fraser; Reuben S. Harris; Valgerður Andrésdóttir; John D. Gross; Nevan J. Krogan

doi:10.1016/j.celrep.2015.04.038

Cell Reports (May 2015)

Lineage-Specific Viral Hijacking of Non-canonical E3 Ubiquitin Ligase Cofactors in the Evolution of Vif Anti-APOBEC3 Activity

Joshua R. Kane,
David J. Stanley,
Judd F. Hultquist,
Jeffrey R. Johnson,
Nicole Mietrach,
Jennifer M. Binning,
Stefán R. Jónsson,
Sarah Barelier,
Billy W. Newton,
Tasha L. Johnson,
Kathleen E. Franks-Skiba,
Ming Li,
William L. Brown,
Hörður I. Gunnarsson,
Adalbjorg Adalbjornsdóttir,
James S. Fraser,
Reuben S. Harris,
Valgerður Andrésdóttir,
John D. Gross,
Nevan J. Krogan

Affiliations

Joshua R. Kane: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
David J. Stanley: Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA
Judd F. Hultquist: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Jeffrey R. Johnson: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Nicole Mietrach: Institute for Experimental Pathology, University of Iceland, Keldur, 112 Reykjavík, Iceland
Jennifer M. Binning: Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA
Stefán R. Jónsson: Institute for Experimental Pathology, University of Iceland, Keldur, 112 Reykjavík, Iceland
Sarah Barelier: Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA
Billy W. Newton: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Tasha L. Johnson: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Kathleen E. Franks-Skiba: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Ming Li: Department of Biochemistry, Molecular Biology and Biophysics, Institute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA
William L. Brown: Department of Biochemistry, Molecular Biology and Biophysics, Institute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA
Hörður I. Gunnarsson: Institute for Experimental Pathology, University of Iceland, Keldur, 112 Reykjavík, Iceland
Adalbjorg Adalbjornsdóttir: Institute for Experimental Pathology, University of Iceland, Keldur, 112 Reykjavík, Iceland
James S. Fraser: California Institute for Quantitative Biosciences, QB3, University of California, San Francisco, San Francisco, CA 94158, USA
Reuben S. Harris: Department of Biochemistry, Molecular Biology and Biophysics, Institute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA
Valgerður Andrésdóttir: Institute for Experimental Pathology, University of Iceland, Keldur, 112 Reykjavík, Iceland
John D. Gross: Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA
Nevan J. Krogan: Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA

DOI: https://doi.org/10.1016/j.celrep.2015.04.038
Journal volume & issue: Vol. 11, no. 8
pp. 1236 – 1250

Abstract

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HIV-1 encodes the accessory protein Vif, which hijacks a host Cullin-RING ubiquitin ligase (CRL) complex as well as the non-canonical cofactor CBFβ, to antagonize APOBEC3 antiviral proteins. Non-canonical cofactor recruitment to CRL complexes by viral factors, to date, has only been attributed to HIV-1 Vif. To further study this phenomenon, we employed a comparative approach combining proteomic, biochemical, structural, and virological techniques to investigate Vif complexes across the lentivirus genus, including primate (HIV-1 and simian immunodeficiency virus macaque [SIVmac]) and non-primate (FIV, BIV, and MVV) viruses. We find that CBFβ is completely dispensable for the activity of non-primate lentiviral Vif proteins. Furthermore, we find that BIV Vif requires no cofactor and that MVV Vif requires a novel cofactor, cyclophilin A (CYPA), for stable CRL complex formation and anti-APOBEC3 activity. We propose modular conservation of Vif complexes allows for potential exaptation of functions through the acquisition of non-CRL-associated host cofactors while preserving anti-APOBEC3 activity.

Published in Cell Reports

ISSN: 2211-1247 (Online)
Publisher: Elsevier
Country of publisher: Netherlands
LCC subjects: Science: Biology (General)
Website: http://www.cell.com/cell-reports/home

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