Myosin light chain 3 serves as a receptor for nervous necrosis virus entry into host cells via the macropinocytosis pathway.

Fuente: PubMed
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Auteurs principaux: Yao, Lan, Zhang, Wanwan, Yang, Xiaogang, Yi, Meisheng, Jia, Kuntong
Format: Artículo científico
Langue:en
Publié: eLife 2025
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author Yao, Lan
Zhang, Wanwan
Yang, Xiaogang
Yi, Meisheng
Jia, Kuntong
author_facet Yao, Lan
Zhang, Wanwan
Yang, Xiaogang
Yi, Meisheng
Jia, Kuntong
Yao, Lan
Zhang, Wanwan
Yang, Xiaogang
Yi, Meisheng
Jia, Kuntong
collection PubMed - marine biology
contents Myosin light chain 3 serves as a receptor for nervous necrosis virus entry into host cells via the macropinocytosis pathway. Yao, Lan Zhang, Wanwan Yang, Xiaogang Yi, Meisheng Jia, Kuntong Animals Pinocytosis Virus Internalization Nodaviridae Myosin Light Chains Oryzias RNA Virus Infections Fish Diseases Receptors, Virus Nodaviridae infections cause severe mortality in insects and fish, with nervous necrosis virus (NNV) posing significant threats to global fish populations. However, the host factors involved in NNV entry remain poorly understood. We identify myosin light chain 3 from marine medaka () (MmMYL3) as a novel receptor for red-spotted grouper NNV (RGNNV), facilitating internalization via macropinocytosis. MmMYL3 directly binds the RGNNV capsid protein (CP), which depends on the arm and S domains of CP and the EF-hand2 domain of MmMYL3. In vitro experiments showed that MmMYL3 siRNA, protein, anti-MYL3 antibodies, or the arm domain synthetic peptides blocked RGNNV entry. Moreover, in vivo administration of MmMYL3 protein also inhibited RGNNV infection. Ectopic MmMYL3 expression enabled RGNNV internalization into resistant cells. Notably, MmMYL3 facilitated RGNNV internalization through the macropinocytosis pathway via the IGF1R-Rac1/Cdc42 axis. Collectively, our findings underscore MYL3's crucial role in NNV entry and its potential as an antiviral target.
format Artículo científico
id pubmed_40560751
institution PubMed
language en
publishDate 2025
publisher eLife
record_format pubmed
spellingShingle Myosin light chain 3 serves as a receptor for nervous necrosis virus entry into host cells via the macropinocytosis pathway.
Yao, Lan
Zhang, Wanwan
Yang, Xiaogang
Yi, Meisheng
Jia, Kuntong
Animals
Pinocytosis
Virus Internalization
Nodaviridae
Myosin Light Chains
Oryzias
RNA Virus Infections
Fish Diseases
Receptors, Virus
Myosin light chain 3 serves as a receptor for nervous necrosis virus entry into host cells via the macropinocytosis pathway. Yao, Lan Zhang, Wanwan Yang, Xiaogang Yi, Meisheng Jia, Kuntong Animals Pinocytosis Virus Internalization Nodaviridae Myosin Light Chains Oryzias RNA Virus Infections Fish Diseases Receptors, Virus Nodaviridae infections cause severe mortality in insects and fish, with nervous necrosis virus (NNV) posing significant threats to global fish populations. However, the host factors involved in NNV entry remain poorly understood. We identify myosin light chain 3 from marine medaka () (MmMYL3) as a novel receptor for red-spotted grouper NNV (RGNNV), facilitating internalization via macropinocytosis. MmMYL3 directly binds the RGNNV capsid protein (CP), which depends on the arm and S domains of CP and the EF-hand2 domain of MmMYL3. In vitro experiments showed that MmMYL3 siRNA, protein, anti-MYL3 antibodies, or the arm domain synthetic peptides blocked RGNNV entry. Moreover, in vivo administration of MmMYL3 protein also inhibited RGNNV infection. Ectopic MmMYL3 expression enabled RGNNV internalization into resistant cells. Notably, MmMYL3 facilitated RGNNV internalization through the macropinocytosis pathway via the IGF1R-Rac1/Cdc42 axis. Collectively, our findings underscore MYL3's crucial role in NNV entry and its potential as an antiviral target.
title Myosin light chain 3 serves as a receptor for nervous necrosis virus entry into host cells via the macropinocytosis pathway.
topic Animals
Pinocytosis
Virus Internalization
Nodaviridae
Myosin Light Chains
Oryzias
RNA Virus Infections
Fish Diseases
Receptors, Virus
url https://pubmed.ncbi.nlm.nih.gov/40560751/