HECT domain interaction with ubiquitin binding sites on Tsg101-UEV controls HIV-1 egress, maturation, and infectivity.


Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
02 2023
Historique:
received: 13 12 2022
revised: 05 01 2023
accepted: 06 01 2023
pubmed: 16 1 2023
medline: 25 2 2023
entrez: 15 1 2023
Statut: ppublish

Résumé

The HECT domain of HECT E3 ligases consists of flexibly linked N- and C-terminal lobes, with a ubiquitin (Ub) donor site on the C-lobe that is directly involved in substrate modification. HECT ligases also possess a secondary Ub binding site in the N-lobe, which is thought to play a role in processivity, specificity, or regulation. Here, we report the use of paramagnetic solution NMR to characterize a complex formed between the isolated HECT domain of neural precursor cell-expressed developmentally downregulated 4-1 and the ubiquitin E2 variant (UEV) domain of tumor susceptibility gene 101 (Tsg101). Both proteins are involved in endosomal trafficking, a process driven by Ub signaling, and are hijacked by viral pathogens for particle assembly; however, a direct interaction between them has not been described, and the mechanism by which the HECT E3 ligase contributes to pathogen formation has not been elucidated. We provide evidence for their association, consisting of multiple sites on the neural precursor cell-expressed developmentally downregulated 4-1 HECT domain and elements of the Tsg101 UEV domain involved in noncovalent ubiquitin binding. Furthermore, we show using an established reporter assay that HECT residues perturbed by UEV proximity define determinants of viral maturation and infectivity. These results suggest the UEV interaction is a determinant of HECT activity in Ub signaling. As the endosomal trafficking pathway is hijacked by several human pathogens for egress, the HECT-UEV interaction could represent a potential novel target for therapeutic intervention.

Identifiants

pubmed: 36642186
pii: S0021-9258(23)00033-9
doi: 10.1016/j.jbc.2023.102901
pmc: PMC9944984
pii:
doi:

Substances chimiques

Endosomal Sorting Complexes Required for Transport 0
Tsg101 protein 0
Ubiquitin 0
Ubiquitin-Protein Ligases EC 2.3.2.27

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

102901

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI150489
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007602
Pays : United States

Informations de copyright

Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.

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Auteurs

David A Nyenhuis (DA)

Biochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.

Rohith Rajasekaran (R)

Biochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.

Susan Watanabe (S)

Department of Microbiology & Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, New York, USA.

Marie-Paule Strub (MP)

Biochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.

Mahfuz Khan (M)

Department of Microbiology & Immunology, Morehouse School of Medicine, Atlanta, Georgia, USA.

Michael Powell (M)

Department of Microbiology & Immunology, Morehouse School of Medicine, Atlanta, Georgia, USA.

Carol A Carter (CA)

Department of Microbiology & Immunology, Renaissance School of Medicine, Stony Brook University, Stony Brook, New York, USA. Electronic address: carol.carter@stonybrook.edu.

Nico Tjandra (N)

Biochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: tjandran@nhlbi.nih.gov.

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