Clinically observed deletions in SARS-CoV-2 Nsp1 affect its stability and ability to inhibit translation
(2022) In FEBS Letters 596(9). p.1203-1213- Abstract
Nonstructural protein 1 (Nsp1) of SARS-CoV-2 inhibits host cell translation through an interaction between its C-terminal domain and the 40S ribosome. The N-terminal domain (NTD) of Nsp1 is a target of recurring deletions, some of which are associated with altered COVID-19 disease progression. Here, we characterize the efficiency of translational inhibition by clinically observed Nsp1 deletion variants. We show that a frequent deletion of residues 79-89 severely reduces the ability of Nsp1 to inhibit translation while not abrogating Nsp1 binding to the 40S. Notably, while the SARS-CoV-2 5' untranslated region enhances translation of mRNA, it does not protect from Nsp1-mediated inhibition. Finally, thermal stability measurements and... (More)
Nonstructural protein 1 (Nsp1) of SARS-CoV-2 inhibits host cell translation through an interaction between its C-terminal domain and the 40S ribosome. The N-terminal domain (NTD) of Nsp1 is a target of recurring deletions, some of which are associated with altered COVID-19 disease progression. Here, we characterize the efficiency of translational inhibition by clinically observed Nsp1 deletion variants. We show that a frequent deletion of residues 79-89 severely reduces the ability of Nsp1 to inhibit translation while not abrogating Nsp1 binding to the 40S. Notably, while the SARS-CoV-2 5' untranslated region enhances translation of mRNA, it does not protect from Nsp1-mediated inhibition. Finally, thermal stability measurements and structure predictions reveal a correlation between stability of the NTD and the efficiency of translation inhibition.
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- author
- Kumar, Pravin ; Schexnaydre, Erin ; Rafie, Karim ; Kurata, Tatsuaki LU ; Terenin, Ilya ; Hauryliuk, Vasili LU and Carlson, Lars-Anders
- organization
- publishing date
- 2022-04-17
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Nsp1, SARS-CoV-2, COVID-19, pathogenicity, ribosome, translation, virus
- in
- FEBS Letters
- volume
- 596
- issue
- 9
- pages
- 1203 - 1213
- publisher
- Wiley-Blackwell
- external identifiers
-
- scopus:85129091882
- pmid:35434785
- ISSN
- 1873-3468
- DOI
- 10.1002/1873-3468.14354
- language
- English
- LU publication?
- yes
- additional info
- This article is protected by copyright. All rights reserved.
- id
- 6077de65-fb43-4101-8278-cc74aba4f0d3
- date added to LUP
- 2022-04-19 11:10:16
- date last changed
- 2024-11-01 02:27:25
@article{6077de65-fb43-4101-8278-cc74aba4f0d3, abstract = {{<p>Nonstructural protein 1 (Nsp1) of SARS-CoV-2 inhibits host cell translation through an interaction between its C-terminal domain and the 40S ribosome. The N-terminal domain (NTD) of Nsp1 is a target of recurring deletions, some of which are associated with altered COVID-19 disease progression. Here, we characterize the efficiency of translational inhibition by clinically observed Nsp1 deletion variants. We show that a frequent deletion of residues 79-89 severely reduces the ability of Nsp1 to inhibit translation while not abrogating Nsp1 binding to the 40S. Notably, while the SARS-CoV-2 5' untranslated region enhances translation of mRNA, it does not protect from Nsp1-mediated inhibition. Finally, thermal stability measurements and structure predictions reveal a correlation between stability of the NTD and the efficiency of translation inhibition.</p>}}, author = {{Kumar, Pravin and Schexnaydre, Erin and Rafie, Karim and Kurata, Tatsuaki and Terenin, Ilya and Hauryliuk, Vasili and Carlson, Lars-Anders}}, issn = {{1873-3468}}, keywords = {{Nsp1; SARS-CoV-2; COVID-19; pathogenicity; ribosome; translation; virus}}, language = {{eng}}, month = {{04}}, number = {{9}}, pages = {{1203--1213}}, publisher = {{Wiley-Blackwell}}, series = {{FEBS Letters}}, title = {{Clinically observed deletions in SARS-CoV-2 Nsp1 affect its stability and ability to inhibit translation}}, url = {{http://dx.doi.org/10.1002/1873-3468.14354}}, doi = {{10.1002/1873-3468.14354}}, volume = {{596}}, year = {{2022}}, }