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

Yao, Defu; Ruan, Lingwei; Xu, Xun; Shi, Hong

doi:10.1016/j.dci.2014.12.012

Cited by 29 publications

(15 citation statements)

References 35 publications

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“…So, it is inferred that under stressed, immune conditions, JNK could translocate from the cytoplasm to the nucleus where it could phosphorylate and activate c-Jun, which in turn could induce the expression of JNK-pathway-target genes. This hypothesis is supported by the observation that JNK-phosphorylation levels are evidently reduced by JNK-inhibitor (SP600125) treatment in vivo (120, 121). More direct evidence should be demonstrated to further explore whether JNK can interact with and phosphorylate c-Jun in vitro (119).…”

Section: The Imd Signaling Pathway In Shrimpmentioning

confidence: 76%

The Two NF-κB Pathways Regulating Bacterial and WSSV Infection of Shrimp

Wang

2019

Front. Immunol.

129

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The outbreak of diseases ordinarily results from the disruption of the balance and harmony between hosts and pathogens. Devoid of adaptive immunity, shrimp rely largely on the innate immune system to protect themselves from pathogenic infection. Two nuclear factor-κB (NF-κB) pathways, the Toll and immune deficiency (IMD) pathways, are generally regarded as the major regulators of the immune response in shrimp, which have been extensively studied over the years. Bacterial infection can be recognized by Toll and IMD pathways, which activate two NF-κB transcription factors, Dorsal and Relish, respectively, to eventually lead to boosting the expression of various antimicrobial peptides (AMPs). In response to white-spot-syndrome-virus (WSSV) infection, these two pathways appear to be subverted and hijacked to favor viral survival. In this review, the recent progress in elucidating microbial recognition, signal transduction, and effector regulation within both shrimp Toll and IMD pathways will be discussed. We will also highlight and discuss the similarities and differences between shrimps and their Drosophila or mammalian counterparts. Understanding the interplay between pathogens and shrimp NF-κB pathways may provide new opportunities for disease-prevention strategies in the future.

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Section: The Imd Signaling Pathway In Shrimpmentioning

confidence: 76%

The Two NF-κB Pathways Regulating Bacterial and WSSV Infection of Shrimp

Wang

2019

Front. Immunol.

129

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“…vannamei VIH-2 inhibits Vg transcript expression in two ways, which include triggering JNK phosphorylation and increasing P 38 MAPK content, while the expected ERK-dependent pathway is not involved (Figs 5 & 6 ). Previous studies have shown that the P 38 MAPK- [ 56 ], ERK- [ 57 ], JNK-dependent cascades [ 58 , 59 ] may be activated (including phosphorylation and/or gene expression) during infection of pathogens. It would be logical to speculate that in shrimp, a complicated signaling complex may be activated in response to pathogenic infection [ 60 , 61 ], which would include the MAPK-dependent cascades, with the side effect of inhibiting vitellogenesis, to save energy and nutrition for against the invasive pathogens.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms for type-II vitellogenesis-inhibiting hormone suppression of vitellogenin transcription in shrimp hepatopancreas: Crosstalk of GC/cGMP pathway with different MAPK-dependent cascades

et al. 2018

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Vitellogenesis is the process of yolk formation via accumulating vitellin (Vn) with nutrients in the oocytes. Expression of vitellogenin (Vg), the precursor of Vn, is one of the indicators for the start of vitellogenesis. In Pacific white shrimp (Litopenaeus vannamei), the type-II vitellogenesis-inhibiting hormone (VIH-2) effectively suppresses hepatopancreatic Vg mRNA expression. In this study, we demonstrate the increasing transcript levels of hepatopancreatic Vg during L. vannamei ovarian development, suggesting that the hepatopancreas-derived Vg/Vn may also contribute to vitellogenesis in this species. Using a combination of in vivo injections and in vitro primary cell cultures, we provide evidences that the inhibition of VIH-2 on hepatopancreatic Vg gene expression is mediated through a functional coupling of the GC/cGMP pathway with different MAPK-dependent cascades in female shrimp. In VIH-2 signaling, the NO-independent GC/cGMP/PKG cascades were upstream of the MAPKs. Activations of the MAPK signal by VIH-2 include the phosphorylation of JNK and the mRNA/protein expression of P38MAPK. Additionally, the cAMP/PKA pathway is another positive intracellular signal for hepatopancreatic Vg mRNA expression but is independent of its VIH-2 regulation. Our findings establish a model for the signal transduction mechanism of Vg regulation by VIH and shed light on the biological functions and signaling of the CHH family in crustaceans.

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“…affecting shrimp [21].It is a baculovirus with double stranded DNA [22], and the mortality rate of WSSV-infected shrimp can reach 100% in 7-10 days. Recently, researchers found another serious shrimp disease (acute hepatopancreatic necrosis disease AHPNS/early mortality syndrome EMS), which is characterised by empty stomach, severe atrophy of hepatopancreas and soft carapace.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Survival and immune response of white shrimp Litopenaeus vannamei following single and concurrent infections with WSSV and Vibrio parahaemolyticus

Pang

Wang

Zhou

et al. 2019

Fish & Shellfish Immunology

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The survival and immune responses of Litopenaeus vannamei were evaluated during white spot syndrome virus (WSSV) or Vibrio parahaemolyticus single and concurrent infections. The mortality, WSSV load, activities of 4 immune enzymes: acid phosphatase (ACP), alkaline phosphatase (AKP), peroxidase (POD) and superoxide dismutase (SOD), and the transcription of Evolutionarily Conserved Signaling Intermediate in Toll pathways of L.vannamei (LvECSIT) were quantified at 0, 3, 6, 12, 24, 48, 72 and 96 h post-infection (pi). The results showed: (i) the cumulative mortality of the co-infection group (WSSV and V. Parahaemolyticus 83 %) was significantly lower than the WSSV infection group (97%) (P < 0.05) at 96 hpi; (ii) copies of WSSV in the co-infection group were significantly lower than that of the single infection group from 24 to 96 hpi (P < 0.05); (iii) ACP, AKP,POD and SOD activity in the gills of the co-infection group was higher than that of the WSSV group at12, 48 and 96 hpi (P < 0.05).The expression of LvECSIT mRNA in the co-infection group was significantly higher than in the WSSV infection group from 12 to72 hpi (P < 0.05).The results indicate that proliferation of WSSV is inhibited by V.parahaemolyticus infection. In addition, infection with WSSV alone causes a significant reduction in some immune responses of shrimp than co-infection with WSSV and V.parahaemolyticus occurs at 26 °C. Third, LvECSIT, an essential member of TLR signaling pathway might play a crucial role in shrimp defense against WSSV-Vibrio co-infection.

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

Cited by 29 publications

References 35 publications

The Two NF-κB Pathways Regulating Bacterial and WSSV Infection of Shrimp

The Two NF-κB Pathways Regulating Bacterial and WSSV Infection of Shrimp

Mechanisms for type-II vitellogenesis-inhibiting hormone suppression of vitellogenin transcription in shrimp hepatopancreas: Crosstalk of GC/cGMP pathway with different MAPK-dependent cascades

Survival and immune response of white shrimp Litopenaeus vannamei following single and concurrent infections with WSSV and Vibrio parahaemolyticus

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