2026-10-15T08:05:11Z https://data.mendeley.com/oai

oai:data.mendeley.com/x9ms3fhc9f.2 2025-09-10T17:22:27Z

Wang, Qing GPR143 directs virus-induced cell vacuolation via the MKK6–p38 pathway Mendeley Data Cytoplasmic vacuolization is observed in vertebrate cells following exposure to viral pathogens. Causing cytoplasmic vacuolization is a key step for many viruses to induce cell death, however, the mechanisms underlying cytoplasmic vacuolization are unclear. Nervous necrosis virus (NNV) induces pronounced cytoplasmic vacuoles in the brain during infection. G protein-coupled receptors (GPCRs) regulate autophagosomes and cause vacuolation. Here, we used grouper and red-spotted grouper NNV (RGNNV) as the model to investigate the role of GPCRs in mediating virus induced cellular vacuolation in the central nervous system. GPR143 enhanced RGNNV-induced cytoplasmic vacuolation through intracellular binding to the RGNNV capsid protein and influenced the binding of autophagosomes and lysosomes. RGNNV enhanced interactions between GPR143 and MKK6, which phosphorylated p38 mitogen-activated protein kinase, subsequently activating the mTOR pathway, augmenting the binding of autophagosomes and lysosomes, and causing cytoplasmic vacuolation. Our study adds a new pathway by which viruses cause vacuolation in vertebrates. Histology Fluorescence Microscopy Western Blot Fluorescence in Situ Hybridization Real-Time Polymerase Chain Reaction Grouper Fish Liang, Jian Tao He, Xuehong Wei, Liyun Yan, Xu Meng, Yanghui Zhu, Xiuru Qing, Songli Zhao, Huihong Gan, Lian Wu, Jinhui Gan, Song Yong Qin, Qi Wei Dataset doi:10.17632/x9ms3fhc9f.2 oai:data.mendeley.com/x9ms3fhc9f.2 Creative Commons Attribution 4.0 International http://creativecommons.org/licenses/by/4.0 https://data.mendeley.com/datasets/x9ms3fhc9f 2025-09-10T17:22:27Z