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Zika Virus Protease Cleavage of Host Protein Septin-2 Mediates Mitotic Defects in Neural Progenitors

Neuron.. 2019;

Li H1, Saucedo-Cuevas L1, Yuan L2, Ross D3, Johansen A1, Sands D3, Stanley V3, Guemez-Gamboa A1, Gregor A1, Evans T4, Chen S4, Tan L4, Molina H5, Sheets N6, Shiryaev SA7, Terskikh AV7, Gladfelter AS8, Shresta S6, Xu Z2, Gleeson JG9.

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Peptide Synthesis	Benzoyl-norleucine-lysine-lysine-arginine 7-amido-4-methylcou-marin (Bz-Nle-Lys-Lys-Arg-AMC; Genscript) was used as substrate to measure protease activity and the efficacy of different NS3 inhibitors.	Get A Quote

摘要

Zika virus (ZIKV) targets neural progenitor cells in the brain, attenuates cell proliferation, and leads to cell death. Here, we describe a role for the ZIKV protease NS2B-NS3 heterodimer in mediating neurotoxicity through cleavage of a host protein required for neurogenesis. Similar to ZIKV infection, NS2B-NS3 expression led to cytokinesis defects and cell death in a protease activity-dependent fashion. Among binding partners, NS2B-NS3 cleaved Septin-2, a cytoskeletal factor involved in cytokinesis. Cleavage of Septin-2 occurred at residue 306 and forced expression of a non-cleavable Septin-2 restored cytokinesis, suggesting a direct mechanism of ZIKV-induced neural toxicity. VIDEO ABSTRACT.,Copyright © 201... More