| Literature DB >> 33590968 |
Joel Selkrig1, Megan Stanifer2, André Mateus1, Karin Mitosch1, Inigo Barrio-Hernandez3, Mandy Rettel4, Heeyoung Kim2, Carlos G P Voogdt1, Philipp Walch1,5, Carmon Kee2, Nils Kurzawa1,5, Frank Stein4, Clément Potel1, Anna Jarzab6, Bernhard Kuster6, Ralf Bartenschlager2,7,8, Steeve Boulant9,10, Pedro Beltrao3, Athanasios Typas1, Mikhail M Savitski1.
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global threat to human health and has compromised economic stability. In addition to the development of an effective vaccine, it is imperative to understand how SARS-CoV-2 hijacks host cellular machineries on a system-wide scale so that potential host-directed therapies can be developed. In situ proteome-wide abundance and thermal stability measurements using thermal proteome profiling (TPP) can inform on global changes in protein activity. Here we adapted TPP to high biosafety conditions amenable to SARS-CoV-2 handling. We discovered pronounced temporal alterations in host protein thermostability during infection, which converged on cellular processes including cell cycle, microtubule and RNA splicing regulation. Pharmacological inhibition of host proteins displaying altered thermal stability or abundance during infection suppressed SARS-CoV-2 replication. Overall, this work serves as a framework for expanding TPP workflows to globally important human pathogens that require high biosafety containment and provides deeper resolution into the molecular changes induced by SARS-CoV-2 infection.Entities:
Keywords: SARS-CoV-2; aryl hydrocarbon hydroxylase; heat shock chaperone; rhapontigenin; tanespimycin
Mesh:
Substances:
Year: 2021 PMID: 33590968 PMCID: PMC7885171 DOI: 10.15252/msb.202010188
Source DB: PubMed Journal: Mol Syst Biol ISSN: 1744-4292 Impact factor: 11.429