Cloning of penaeidin gene promoter in tiger shrimp (Penaeus monodon)

Ho, Shih-Hu; Song, Yen-Ling

doi:10.1016/j.fsi.2009.05.001

Cited by 29 publications

(14 citation statements)

References 23 publications

(40 reference statements)

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“…The luciferase reporter vectors pGL3-PEN453, pGL3-PEN309, pGL3-PEN4, pGL3-Drs or pGL3-AttA were constructed in previous studies and demonstrated to be regulated predominantly through NF-κB activation. 18,19,21,28,29,30 Using the same method, 147 WSSV luciferase reporters were constructed as described previously. 25,31 An NF-κB luciferase reporter (Clontech) was used to study NF-κB signaling in HEK 293T cells.…”

Section: Methodsmentioning

confidence: 99%

The shrimp IKK–NF-κB signaling pathway regulates antimicrobial peptide expression and may be subverted by white spot syndrome virus to facilitate viral gene expression

Wang

Wan

et al. 2013

Cell Mol Immunol

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The IκB kinases IKKα and IKKβ and the IKK-related kinases TANK-binding kinase 1 (TBK1) and IKKε are the master regulators of the NF-κB signaling pathway. Although this pathway has been extensively studied in mammals, less attention has been paid in crustaceans, which have significant economic value. Here, we report the cloning and functional studies of two IKK homologs, LvIKKβ and LvIKKε, from Pacific white shrimp, Litopenaeus vannamei. LvIKKβ and LvIKKε mRNAs are widely expressed in different tissues and are responsive to white spot syndrome virus (WSSV) infection. When overexpressed in Drosophila S2 cells, LvIKKβ but not LvIKKε activates the promoters of NF-κB pathway-controlled antimicrobial peptide genes (AMPs), such as the Penaeidins (PENs). In HEK 293T cells, both LvIKKβ and LvIKKε activate an NF-κB reporter. The silencing of LvIKKβ or LvIKKε using double-stranded RNA (dsRNA)-mediated RNA interference (RNAi) decreases the expression of L. vannamei AMPs, including PENs, lysozyme and crustins. Intriguingly, LvIKKβ- or LvIKKε-silenced L. vannamei are resistant to WSSV infection. We hypothesized that successful infection with WSSV requires the activation of the IKK–NF-κB signaling pathway to modulate viral gene expression. We constructed luciferase reporters for 147 WSSV genes. By screening, we found that the WSV051, WSV059, WSV069, WSV083, WSV090, WSV107, WSV244, WSV303, WSV371 and WSV445 promoters can be activated by LvIKKβ or LvIKKε in Drosophila S2 cells. Taken together, our results reveal that LvIKKβ and LvIKKε may participate in the regulation of shrimp AMPs and that WSSV may subvert the L. vannamei IKK–NF-κB signaling pathway to facilitate viral gene expression.

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Section: Methodsmentioning

confidence: 99%

The shrimp IKK–NF-κB signaling pathway regulates antimicrobial peptide expression and may be subverted by white spot syndrome virus to facilitate viral gene expression

Wang

Wan

et al. 2013

Cell Mol Immunol

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“…The complete LvIAP1-3 open reading frames (ORFs) were inserted into the pAc5.1-N-GFP vector to create the pAc5.1-LvIAP1-3-GFP, expressing full-length LvIAP1-3 fused with GFP. The luciferase reporter vectors, including pGL3-PEN453, pGL3-PEN309, pGL3-PEN4, pGL3-Drs, pGL3-AttA, pGL3-WSSV069, pGL3-WSSV303, and pGL3-WSSV371, had been constructed in previous studies [44,47] and were predominantly regulated through NF-κB activation [45,47,49–52]. The promoter sequences of PEN453, PEN309, PEN4, Drs, AttA, WSSV069, WSSV303, and WSSV371 are provided in Figure S1.…”

Section: Methodsmentioning

confidence: 99%

Analysis of Expression, Cellular Localization, and Function of Three Inhibitors of Apoptosis (IAPs) from Litopenaeus vannamei during WSSV Infection and in Regulation of Antimicrobial Peptide Genes (AMPs)

Wang

Wan

et al. 2013

PLoS ONE

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Inhibitors of apoptosis (IAPs) play important roles in apoptosis and NF-κB activation. In this study, we cloned and characterized three IAPs (LvIAP1-3) from the Pacific white shrimp, Litopenaeusvannamei . LvIAP1-3 proteins shared signature domains and exhibited significant similarities with other IAP family proteins. The tissue distributions of LvIAP1-3 were studied. The expression of LvIAP1-3 was induced in the muscle after white spot syndrome virus (WSSV) infection. LvIAP1 expression in the gill, hemocytes, hepatopancreas, and intestine was responsive to WSSV and Vibrio alginolyticus infections. LvIAP2 expression in the gill, hemocytes, and hepatopancreas was also responsive to WSSV infection. The expression of LvIAP3 in the gill, hemocytes, and intestine was reduced after V . alginolyticus infection. When overexpressed in Drosophila S2 cells, GFP labeled-LvIAP2 was distributed in the cytoplasm and appeared as speck-like aggregates in the nucleus. Both LvIAP1 and LvIAP3 were widely distributed throughout the cytoplasm and nucleus. The expression of LvIAP1, LvIAP2, and LvIAP3 was significantly knocked down by dsRNA-mediated gene silencing. In the gill of LvIAP1- or LvIAP3-silenced shrimp, the expression of WSSV VP28 was significantly higher than that of the dsGFP control group, suggesting that LvIAP1 and LvIAP3 may play protective roles in host defense against WSSV infection. Intriguingly, the LvIAP2-silenced shrimp all died within 48 hours after dsLvIAP2 injection. In the hemocytes of LvIAP2-silenced shrimps, the expression of antimicrobial peptide genes (AMPs), including Penaeidins, lysozyme, crustins, Vibrio penaeicidae-induced cysteine and proline-rich peptides (VICPs), was significantly downregulated, while the expression of anti-lipopolysaccharide factors (ALFs) was upregulated. Moreover, LvIAP2 activated the promoters of the NF-κB pathway-controlled AMPs, such as shrimp Penaeidins and Drosophila drosomycin and attacin A, in Drosophila S2 cells. Taken together, these results reveal that LvIAP1 and LvIAP3 might participate in the host defense against WSSV infection, and LvIAP2 might be involved in the regulation of shrimp AMPs.

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“…In our previous studies [37]–[42], several luciferase reporter vectors were constructed using the promoter sequences of following genes: the Drosophila AMPs, Attacin A (AttA), Drosomycin (Drs), and Metchnikowin (Mtk); the L. vannamei AMP Penaeidin4 (PEN4); the Penaeus monodon AMP Penaeidin (PEN309, PEN453, and PEN536); and wsv069 (ie1), wsv303, and wsv371. Luciferase reporter genes, including pGL3-AttA, pGL3-Drs, pGL3-Mtk, pGL3-PEN4, pGL3-PEN309, pGL3-PEN453, pGL3-PEN536, pGL3-wsv069, pGL3-wsv303, and pGL3-wsv371, have been shown to be regulated through NF-κB activation [37], [39], [40], [44]–[46].…”

Section: Methodsmentioning

confidence: 99%

Identification and Function of Myeloid Differentiation Factor 88 (MyD88) in Litopenaeus vannamei

Zhang

Yan

et al. 2012

PLoS ONE

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Myeloid differentiation factor 88 (MyD88) is a universal and essential signaling protein in Toll-like receptor/interleukin-1 receptor-induced activation of nuclear factor-kappa B. In this study, two MyD88 protein variants (LvMyD88 and LvMyD88-1) were identified in Litopenaeus vannamei. The LvMyD88 cDNA is 1,848 bp in length and contains an open reading frame (ORF) of 1,428 bp, whereas the LvMyD88-1 cDNA is 1,719 bp in length and has an ORF of 1,299 bp. Both variants encode proteins with death and Toll/interleukin-1 receptor domains and share 91% sequence identity. In healthy L. vannamei, the LvMyD88 genes were highly expressed in hemocytes but at a low level in the hepatopancreas. The LvMyD88s expression was induced in hemocytes after challenge with lipopolysaccharide, CpG-ODN2006, Vibrio parahaemolyticus, Staphyloccocus aureus, and white spot syndrome virus, but not by poly I∶C. Overexpression of LvMyD88 and LvMyD88-1 in Drosophila Schneider 2 cells led to activation of antimicrobial peptide genes and wsv069 (ie1), wsv303, and wsv371. These results suggested that LvMyD88 may play a role in antibacterial and antiviral response in L. vannamei. To our knowledge, this is the first report on MyD88 in shrimp and a variant of MyD88 gene in invertebrates.

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Cloning of penaeidin gene promoter in tiger shrimp (Penaeus monodon)

Cited by 29 publications

References 23 publications

The shrimp IKK–NF-κB signaling pathway regulates antimicrobial peptide expression and may be subverted by white spot syndrome virus to facilitate viral gene expression

The shrimp IKK–NF-κB signaling pathway regulates antimicrobial peptide expression and may be subverted by white spot syndrome virus to facilitate viral gene expression

Analysis of Expression, Cellular Localization, and Function of Three Inhibitors of Apoptosis (IAPs) from Litopenaeus vannamei during WSSV Infection and in Regulation of Antimicrobial Peptide Genes (AMPs)

Identification and Function of Myeloid Differentiation Factor 88 (MyD88) in Litopenaeus vannamei

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