An adaptor protein CRK mediates antiviral immunity against white spot syndrome virus via JAK/STAT signaling pathway in Cherax quadricarinatus.

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Autores principales: Fan, Zi-Han, Liu, Ling-Ke, Wu, Wen-Lin, Liu, Hai-Peng
Formato: Artículo científico
Lenguaje:en
Publicado: Fish & shellfish immunology 2026
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author Fan, Zi-Han
Liu, Ling-Ke
Wu, Wen-Lin
Liu, Hai-Peng
author_facet Fan, Zi-Han
Liu, Ling-Ke
Wu, Wen-Lin
Liu, Hai-Peng
Fan, Zi-Han
Liu, Ling-Ke
Wu, Wen-Lin
Liu, Hai-Peng
collection PubMed - marine biology
contents An adaptor protein CRK mediates antiviral immunity against white spot syndrome virus via JAK/STAT signaling pathway in Cherax quadricarinatus. Fan, Zi-Han Liu, Ling-Ke Wu, Wen-Lin Liu, Hai-Peng Animals White spot syndrome virus 1 Astacoidea Immunity, Innate Signal Transduction Arthropod Proteins Phylogeny Amino Acid Sequence Gene Expression Regulation Sequence Alignment Proto-Oncogene Proteins c-crk Gene Expression Profiling STAT Transcription Factors Base Sequence The CT10 regulator of kinase (CRK) family adaptor proteins are key mediators of intracellular signaling, linking multiple signaling molecules through their Src homology (SH) 2 and SH3 domains. They regulate essential cellular processes, including cell adhesion, migration, phagocytosis, and apoptosis, and are critically involved in host immune signaling during viral infection. However, the function of CRK in white spot syndrome virus (WSSV) infection remains largely unknown in crustaceans. In the present study, a CRK family adaptor protein from the crayfish Cherax quadricarinatus (CqCRK) was identified and characterized. The gene contains an 807 bp open reading frame encoding a 268 amino acid protein with one SH2 domain and two SH3 domains, consistent with conserved CRK family features. Analysis of tissue distribution revealed that CqCRK was broadly expressed, with the highest levels in hemocytes. Upon WSSV infection, CqCRK mRNA expression significantly increased at 24 hpi. Knockdown of CqCRK expression significantly increased viral VP28 expression, indicating that CqCRK suppresses WSSV replication in crayfish and contributes to antiviral immunity. Mechanistically, CqCRK interacts with phosphorylated CqSTAT; meanwhile, gene silencing of CqCRK promotes the accumulation of phosphorylated CqSTAT in the cytoplasm and impairs its nuclear translocation. In addition, CqCRK inhibited the expression of apoptosis related factors, including Cqp53 and CqCaspase1, as well as crayfish hemocyte apoptosis. Collectively, these findings suggest that CqCRK contributes to antiviral defense against WSSV by facilitating the nuclear translocation of CqSTAT and suppressing apoptosis in the late stages of viral infection, thereby shedding new light on the molecular mechanisms underlying antiviral immunity in crustaceans.
format Artículo científico
id pubmed_42009210
institution PubMed
language en
publishDate 2026
publisher Fish & shellfish immunology
record_format pubmed
spellingShingle An adaptor protein CRK mediates antiviral immunity against white spot syndrome virus via JAK/STAT signaling pathway in Cherax quadricarinatus.
Fan, Zi-Han
Liu, Ling-Ke
Wu, Wen-Lin
Liu, Hai-Peng
Animals
White spot syndrome virus 1
Astacoidea
Immunity, Innate
Signal Transduction
Arthropod Proteins
Phylogeny
Amino Acid Sequence
Gene Expression Regulation
Sequence Alignment
Proto-Oncogene Proteins c-crk
Gene Expression Profiling
STAT Transcription Factors
Base Sequence
An adaptor protein CRK mediates antiviral immunity against white spot syndrome virus via JAK/STAT signaling pathway in Cherax quadricarinatus. Fan, Zi-Han Liu, Ling-Ke Wu, Wen-Lin Liu, Hai-Peng Animals White spot syndrome virus 1 Astacoidea Immunity, Innate Signal Transduction Arthropod Proteins Phylogeny Amino Acid Sequence Gene Expression Regulation Sequence Alignment Proto-Oncogene Proteins c-crk Gene Expression Profiling STAT Transcription Factors Base Sequence The CT10 regulator of kinase (CRK) family adaptor proteins are key mediators of intracellular signaling, linking multiple signaling molecules through their Src homology (SH) 2 and SH3 domains. They regulate essential cellular processes, including cell adhesion, migration, phagocytosis, and apoptosis, and are critically involved in host immune signaling during viral infection. However, the function of CRK in white spot syndrome virus (WSSV) infection remains largely unknown in crustaceans. In the present study, a CRK family adaptor protein from the crayfish Cherax quadricarinatus (CqCRK) was identified and characterized. The gene contains an 807 bp open reading frame encoding a 268 amino acid protein with one SH2 domain and two SH3 domains, consistent with conserved CRK family features. Analysis of tissue distribution revealed that CqCRK was broadly expressed, with the highest levels in hemocytes. Upon WSSV infection, CqCRK mRNA expression significantly increased at 24 hpi. Knockdown of CqCRK expression significantly increased viral VP28 expression, indicating that CqCRK suppresses WSSV replication in crayfish and contributes to antiviral immunity. Mechanistically, CqCRK interacts with phosphorylated CqSTAT; meanwhile, gene silencing of CqCRK promotes the accumulation of phosphorylated CqSTAT in the cytoplasm and impairs its nuclear translocation. In addition, CqCRK inhibited the expression of apoptosis related factors, including Cqp53 and CqCaspase1, as well as crayfish hemocyte apoptosis. Collectively, these findings suggest that CqCRK contributes to antiviral defense against WSSV by facilitating the nuclear translocation of CqSTAT and suppressing apoptosis in the late stages of viral infection, thereby shedding new light on the molecular mechanisms underlying antiviral immunity in crustaceans.
title An adaptor protein CRK mediates antiviral immunity against white spot syndrome virus via JAK/STAT signaling pathway in Cherax quadricarinatus.
topic Animals
White spot syndrome virus 1
Astacoidea
Immunity, Innate
Signal Transduction
Arthropod Proteins
Phylogeny
Amino Acid Sequence
Gene Expression Regulation
Sequence Alignment
Proto-Oncogene Proteins c-crk
Gene Expression Profiling
STAT Transcription Factors
Base Sequence
url https://pubmed.ncbi.nlm.nih.gov/42009210/