Société Française de Biochimie et Biologie Moléculaire

DECEMBER 2022 - Limei ZOU

Cell Structural Biology (BIOC),Polytechnique School "The SARS-CoV-2 protein NSP2 impairs the silencing capacity of the human 4EHP-GIGYF2 complex." iScience, 25: 104646. DOI: 10.1016/j.isci.2022.104646
Limei Zou, Clara Moch, Marc Graille & Clément Chapat


Limei ZOU, 31 year-old, is a third-year Ph.D student in the Laboratory of Structural Biology of the Cell (UMR 7654 BIOC) at Ecole Polytechnique (Palaiseau) under the supervision of Dr. Clément Chapat and Dr. Marc Graille. She came from China with a master’s degree in microbiology to pursue a PhD in France with the support of China Scholarship Council. She is presently focusing on the exploration of a novel translational repression mechanism orchestrated by the CCR4-NOT complex in the translation of methylated mRNAs. She has also finalized a research project exploring how the SARS-CoV-2 protein NSP2 impairs the post-transcriptional repression capacities of human cells. Overall, her Ph.D research involves a combined approach, whereby biochemical and functional knowledge derived from cell biology and proteomics will provide insight into how mRNA silencing machineries shape the human proteome.



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Résumé de l'article

There is an urgent need for a molecular understanding of how SARS-CoV-2 influences the machineries of the host cell. Herein, we focused our attention on the capacity of the SARS-CoV-2 protein NSP2 to bind the human 4EHP-GIGYF2 complex, a key factor involved in microRNA-mediated silencing of gene expression. Using in vitro interaction assays, our data demonstrate thatNSP2 physically associates with both 4EHP and a central segment in GIGYF2 in the cytoplasm. We also provide functional evidence showing that NSP2 impairs the function of GIGYF2 in mediating translation repression using reporter-based assays. Collectively, these data reveal the potential impact of NSP2 on the post-transcriptional silencing of gene expression in human cells, pointing out 4EHP-GIGYF2 targeting as a possible strategy of SARS-CoV-2 to take over the silencing machinery and to suppress host defenses.