TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry

SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (...

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Veröffentlicht in:Cell Jg. 186; H. 16; S. 3427
Hauptverfasser: Baggen, Jim, Jacquemyn, Maarten, Persoons, Leentje, Vanstreels, Els, Pye, Valerie E, Wrobel, Antoni G, Calvaresi, Valeria, Martin, Stephen R, Roustan, Chloë, Cronin, Nora B, Reading, Eamonn, Thibaut, Hendrik Jan, Vercruysse, Thomas, Maes, Piet, De Smet, Frederik, Yee, Angie, Nivitchanyong, Toey, Roell, Marina, Franco-Hernandez, Natalia, Rhinn, Herve, Mamchak, Alusha Andre, Ah Young-Chapon, Maxime, Brown, Eric, Cherepanov, Peter, Daelemans, Dirk
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 03.08.2023
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ISSN:1097-4172, 1097-4172
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Abstract SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (ACE2)-negative cells. Spike substitution E484D increased TMEM106B binding, thereby enhancing TMEM106B-mediated entry. TMEM106B-specific monoclonal antibodies blocked SARS-CoV-2 infection, demonstrating a role of TMEM106B in viral entry. Using X-ray crystallography, cryogenic electron microscopy (cryo-EM), and hydrogen-deuterium exchange mass spectrometry (HDX-MS), we show that the luminal domain (LD) of TMEM106B engages the receptor-binding motif of SARS-CoV-2 spike. Finally, we show that TMEM106B promotes spike-mediated syncytium formation, suggesting a role of TMEM106B in viral fusion. Together, our findings identify an ACE2-independent SARS-CoV-2 infection mechanism that involves cooperative interactions with the receptors heparan sulfate and TMEM106B.
AbstractList SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (ACE2)-negative cells. Spike substitution E484D increased TMEM106B binding, thereby enhancing TMEM106B-mediated entry. TMEM106B-specific monoclonal antibodies blocked SARS-CoV-2 infection, demonstrating a role of TMEM106B in viral entry. Using X-ray crystallography, cryogenic electron microscopy (cryo-EM), and hydrogen-deuterium exchange mass spectrometry (HDX-MS), we show that the luminal domain (LD) of TMEM106B engages the receptor-binding motif of SARS-CoV-2 spike. Finally, we show that TMEM106B promotes spike-mediated syncytium formation, suggesting a role of TMEM106B in viral fusion. Together, our findings identify an ACE2-independent SARS-CoV-2 infection mechanism that involves cooperative interactions with the receptors heparan sulfate and TMEM106B.SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (ACE2)-negative cells. Spike substitution E484D increased TMEM106B binding, thereby enhancing TMEM106B-mediated entry. TMEM106B-specific monoclonal antibodies blocked SARS-CoV-2 infection, demonstrating a role of TMEM106B in viral entry. Using X-ray crystallography, cryogenic electron microscopy (cryo-EM), and hydrogen-deuterium exchange mass spectrometry (HDX-MS), we show that the luminal domain (LD) of TMEM106B engages the receptor-binding motif of SARS-CoV-2 spike. Finally, we show that TMEM106B promotes spike-mediated syncytium formation, suggesting a role of TMEM106B in viral fusion. Together, our findings identify an ACE2-independent SARS-CoV-2 infection mechanism that involves cooperative interactions with the receptors heparan sulfate and TMEM106B.
SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (ACE2)-negative cells. Spike substitution E484D increased TMEM106B binding, thereby enhancing TMEM106B-mediated entry. TMEM106B-specific monoclonal antibodies blocked SARS-CoV-2 infection, demonstrating a role of TMEM106B in viral entry. Using X-ray crystallography, cryogenic electron microscopy (cryo-EM), and hydrogen-deuterium exchange mass spectrometry (HDX-MS), we show that the luminal domain (LD) of TMEM106B engages the receptor-binding motif of SARS-CoV-2 spike. Finally, we show that TMEM106B promotes spike-mediated syncytium formation, suggesting a role of TMEM106B in viral fusion. Together, our findings identify an ACE2-independent SARS-CoV-2 infection mechanism that involves cooperative interactions with the receptors heparan sulfate and TMEM106B.
Author Cherepanov, Peter
Calvaresi, Valeria
Reading, Eamonn
De Smet, Frederik
Daelemans, Dirk
Pye, Valerie E
Rhinn, Herve
Maes, Piet
Brown, Eric
Yee, Angie
Vanstreels, Els
Martin, Stephen R
Ah Young-Chapon, Maxime
Baggen, Jim
Cronin, Nora B
Roustan, Chloë
Wrobel, Antoni G
Jacquemyn, Maarten
Vercruysse, Thomas
Mamchak, Alusha Andre
Persoons, Leentje
Nivitchanyong, Toey
Franco-Hernandez, Natalia
Thibaut, Hendrik Jan
Roell, Marina
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Keywords SARS-CoV-2
TMEM106B crystal structure
ACE2-independent entry
antibody neutralization
TMEM106B
coronavirus
cryo-EM
entry receptor
Language English
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References 37541193 - Cell. 2023 Aug 3;186(16):3329-3331. doi: 10.1016/j.cell.2023.07.005.
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Snippet SARS-CoV-2 is associated with broad tissue tropism, a characteristic often determined by the availability of entry receptors on host cells. Here, we show that...
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SubjectTerms Angiotensin-Converting Enzyme 2 - metabolism
COVID-19
Humans
Membrane Proteins - metabolism
Nerve Tissue Proteins - metabolism
Protein Binding
Receptors, Virus - metabolism
SARS-CoV-2 - metabolism
Virus Internalization
Title TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry
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