A novel JNK from Litopenaeus vannamei involved in white spot syndrome virus infection

Shi, Hong; Yan, Xin-Fu; Ruan, Lingwei; Xu, Xun

doi:10.1016/j.dci.2012.03.002

Cited by 49 publications

(18 citation statements)

References 29 publications

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“…Integrin and SDC are regarded as membrane receptors. Interaction of WSSV-CLP with integrin or SDC might lead to the regulation of actin for cell motility or initiate the intracellular signaling pathways, such as MAPK, NF-kappa B signaling pathway, which are responsive to WSSV challenge in shrimp [35–38]. …”

Section: Discussionmentioning

confidence: 99%

Bioinformatic Prediction of WSSV-Host Protein-Protein Interaction

Sun

et al. 2014

BioMed Research International

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WSSV is one of the most dangerous pathogens in shrimp aquaculture. However, the molecular mechanism of how WSSV interacts with shrimp is still not very clear. In the present study, bioinformatic approaches were used to predict interactions between proteins from WSSV and shrimp. The genome data of WSSV (NC_003225.1) and the constructed transcriptome data of F. chinensis were used to screen potentially interacting proteins by searching in protein interaction databases, including STRING, Reactome, and DIP. Forty-four pairs of proteins were suggested to have interactions between WSSV and the shrimp. Gene ontology analysis revealed that 6 pairs of these interacting proteins were classified into “extracellular region” or “receptor complex” GO-terms. KEGG pathway analysis showed that they were involved in the “ECM-receptor interaction pathway.” In the 6 pairs of interacting proteins, an envelope protein called “collagen-like protein” (WSSV-CLP) encoded by an early virus gene “wsv001” in WSSV interacted with 6 deduced proteins from the shrimp, including three integrin alpha (ITGA), two integrin beta (ITGB), and one syndecan (SDC). Sequence analysis on WSSV-CLP, ITGA, ITGB, and SDC revealed that they possessed the sequence features for protein-protein interactions. This study might provide new insights into the interaction mechanisms between WSSV and shrimp.

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Section: Discussionmentioning

confidence: 99%

Bioinformatic Prediction of WSSV-Host Protein-Protein Interaction

Sun

et al. 2014

BioMed Research International

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“…In shrimp, several transcription factors including relish, STAT, Kruppel-like factor, ATF4 and XBP1 were identified to participate in WSSV pathogenesis and viral gene expression (Chang et al, 2012;Huang et al, 2010;Li et al, 2013;Liu et al, 2007). Notably, our previous studies demonstrated that inhibition of shrimp JNK signaling pathway could restrict WSSV replication and delay viral gene expression (Shi et al, 2012). Therefore, it is reasonable to hypothesize that Lvc-Jun probably participates in WSSV gene expression as a downstream effector of JNK.…”

Section: Discussionmentioning

confidence: 94%

“…In shrimp, it has been documented that cellular signaling pathways, such as NF-κB and JAK-STAT, were annexed by WSSV for its replication and gene expression (Huang et al, 2010;Liu et al, 2007). Moreover, previous evidences in our group have established that Litopenaeus vannamei c-Jun N-terminal kinase (LvJNK), one well characterized subfamily of mitogen-activated protein kinases (MAPKs) (Johnson and Lapadat, 2002), was triggered at the early phase of WSSV infection to achieve the same effects (Shi et al, 2012). However, the mechanisms by which LvJNK mediates WSSV infection remain unknown.…”

Section: Introductionmentioning

confidence: 89%

Identification of a c-Jun homolog from Litopenaeus vannamei as a downstream substrate of JNK in response to WSSV infection

Yao

Ruan

et al. 2015

Developmental & Comparative Immunology

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“…In Bombyx mori , the magnitude and pattern of JNK activation were dependent on the multiplicity of nucleopolyhedrovirus infection, and inhibition of JNK reduced occlusion body formation and budded virus production (Katsuma et al, 2007). In a crustacean, Litopenaeus vannamei , JNK was activated in response to white spot syndrome virus infection and the virus proliferation benefited from JNK activation (Shi et al, 2012). Although this phenotype is common in virus–vector and virus–host systems, there should be some mechanisms in vector insects to limit the virus replication to a sustainable level.…”

Section: Discussionmentioning

confidence: 99%

The c-Jun N-terminal kinase pathway of a vector insect is activated by virus capsid protein and promotes viral replication

Wang

Zhao

et al. 2017

eLife

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No evidence has shown whether insect-borne viruses manipulate the c-Jun N-terminal kinase (JNK) signaling pathway of vector insects. Using a system comprising the plant virus Rice stripe virus (RSV) and its vector insect, the small brown planthopper, we have studied the response of the vector insect’s JNK pathway to plant virus infection. We found that RSV increased the level of Tumor Necrosis Factor-α and decreased the level of G protein Pathway Suppressor 2 (GPS2) in the insect vector. The virus capsid protein competitively bound GPS2 to release it from inhibiting the JNK activation machinery. We confirmed that JNK activation promoted RSV replication in the vector, whereas JNK inhibition caused a significant reduction in virus production and thus delayed the disease incidence of plants. These findings suggest that inhibition of insect vector JNK may be a useful strategy for controling the transmission of plant viruses.DOI: http://dx.doi.org/10.7554/eLife.26591.001

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A novel JNK from Litopenaeus vannamei involved in white spot syndrome virus infection

Cited by 49 publications

References 29 publications

Bioinformatic Prediction of WSSV-Host Protein-Protein Interaction

Bioinformatic Prediction of WSSV-Host Protein-Protein Interaction

Identification of a c-Jun homolog from Litopenaeus vannamei as a downstream substrate of JNK in response to WSSV infection

The c-Jun N-terminal kinase pathway of a vector insect is activated by virus capsid protein and promotes viral replication

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