Expression characterization, genomic structure and function analysis of fish ubiquitin-specific protease 18 (USP18) genes

Chen, Chen; Zhang, Yibing; Gui, Jian‐Fang

doi:10.1016/j.dci.2015.05.003

Cited by 12 publications

(4 citation statements)

References 48 publications

(60 reference statements)

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“…As the first defense line of host, IFN system plays a vital role in resistance to viral infection [47]. From UV-inactivated GCHV-infected CAB cells, about 20 IFN system genes, such as TLR3 , IFN , IRF1 [49], IRF3 [50], IRF7 [51], IRF9 [52], signal transducer and activator of transcription 1 ( STAT1 ) [53], mediator of IRF3 activation ( MITA ) [54], Mx1 and Mx2 [55], PKR , PKZ [56], PKR-like [57], IFI58 and IFI56 [58], Gig1 and Gig2 [59], ISG15–1 and ISG15–2 [60], viperin [61], ubiquitin-specific protease 18 ( USP18 ) [62] were identified. Similar to mammalian [86], fish initiates IFN response through recognizing viral products via TLRs and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), then triggers IRF3/7-dependent IFN response [10, 47, 87–89].…”

Section: Discussionmentioning

confidence: 99%

Distinct herpesvirus resistances and immune responses of three gynogenetic clones of gibel carp revealed by comprehensive transcriptomes

et al. 2017

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BackgroundGibel carp is an important aquaculture species in China, and a herpesvirus, called as Carassius auratus herpesvirus (CaHV), has hampered the aquaculture development. Diverse gynogenetic clones of gibel carp have been identified or created, and some of them have been used as aquaculture varieties, but their resistances to herpesvirus and the underlying mechanism remain unknown.ResultsTo reveal their susceptibility differences, we firstly performed herpesvirus challenge experiments in three gynogenetic clones of gibel carp, including the leading variety clone A+, candidate variety clone F and wild clone H. Three clones showed distinct resistances to CaHV. Moreover, 8772, 8679 and 10,982 differentially expressed unigenes (DEUs) were identified from comparative transcriptomes between diseased individuals and control individuals of clone A+, F and H, respectively. Comprehensive analysis of the shared DEUs in all three clones displayed common defense pathways to the herpesvirus infection, activating IFN system and suppressing complements. KEGG pathway analysis of specifically changed DEUs in respective clones revealed distinct immune responses to the herpesvirus infection. The DEU numbers identified from clone H in KEGG immune-related pathways, such as “chemokine signaling pathway”, “Toll-like receptor signaling pathway” and others, were remarkably much more than those from clone A+ and F. Several IFN-related genes, including Mx1, viperin, PKR and others, showed higher increases in the resistant clone H than that in the others. IFNphi3, IFI44-like and Gig2 displayed the highest expression in clone F and IRF1 uniquely increased in susceptible clone A+. In contrast to strong immune defense in resistant clone H, susceptible clone A+ showed remarkable up-regulation of genes related to apoptosis or death, indicating that clone A+ failed to resist virus offensive and evidently induced apoptosis or death.ConclusionsOur study is the first attempt to screen distinct resistances and immune responses of three gynogenetic gibel carp clones to herpesvirus infection by comprehensive transcriptomes. These differential DEUs, immune-related pathways and IFN system genes identified from susceptible and resistant clones will be beneficial to marker-assisted selection (MAS) breeding or molecular module-based resistance breeding in gibel carp.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-017-3945-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Distinct herpesvirus resistances and immune responses of three gynogenetic clones of gibel carp revealed by comprehensive transcriptomes

et al. 2017

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“…OASL2 dysregulation may interrupt activation and migration of macrophage in the HD mouse model or interaction with mHTT fragments in immunological manners. USP18 (ubiquitinspecific protease 18) is an interferon-inducible protein and participate in regulation of interferon response on viral infection (Chen et al, 2015). Goldmann et al (2015) demonstrate that Usp18 is essentially contributedto microglial quiescence in white matter microglia.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of the molecular mechanism underlying Huntington's disease

Wang

Dong

Cong

2019

Journal of Integrative Neuroscience

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We explore the underlying molecular mechanisms and to identify key molecules in Huntington's disease by utilizing bioinformatics methods. The gene expression profile of GSE3621 was extracted from the gene expression omnibus. Differentially expressed genes between the R6/1 transgenic mouse model of Huntington's disease and controls at different time points were screened by limma package in R. Kyoto encyclopedia of genes and genomes database. It was used to analyze the pathways of differentially expressed genes. A searching tool of the proteinprotein interaction network was constructed and visualized by Cytoscape. Molecular complex detection was utilized to performed module analysis. There were 513, 483, and 528 differentially expressed genes identified at weeks 18, 22 and 27, respectively, when compared with the control samples. Also, 24 significantly enriched R. Kyoto encyclopedia of genes and genomes database pathways were identified (9 in week 18, 6 in week 22, 9 in week 27), and 31 significant modules were identified from the protein-protein interaction network (13 in week 18, 8 in week 22, 10 in week 27). Hoxd8, Atf3, and Egr2 were confirmed as transcription factors related to Huntington's disease. There are widespread gene expression changes in Huntington's disease at different time points. Some hub genes, such as Usp18, Oasl2, and Rtp4, may play important roles in the pathogenesis of Huntington's disease.

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“…Recent studies have shown that in mammals, USP18 blocks the activation of the JAK-STAT signaling pathway by Rickettsia conorii infection and inhibits the antiviral action of IFN-I (Colonne, Sahni A., & Sahni S. K., 2013). Other studies have demonstrated that expression of fish and mouse USP18 can inhibit the antiviral response of IFN (Chen et al, 2015;. Besides, other studies have shown that USP18, as a type I IFN-responsive gene, could be rapidly upregulated by IFN-β treatment through the JAK/STAT kinase pathway (Xie et al, 2012 (Yang et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, several studies have suggested that USP18 acts as a negative regulator in mammals, birds and fish (Chen, Zhang, & Gui, 2015;Kang, Jiang, Wu, Pestka, & Fisher, 2001;Malakhova et al, 2006;Wei, Wei, & Zhou, 2016). In mice, USP18 negatively regulates IFN signaling, independent of its isopeptidase activity associated with ISG15, by binding to the IFNAR2 receptor subunit and blocking the interaction between Janus kinase and the IFN receptor (Malakhova et al, 2006).…”

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Negative regulation of the RLR‐mediated IFN signaling pathway by duck ubiquitin‐specific protease 18 (USP18)

et al. 2018

Journal Cellular Physiology

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Ubiquitin-specific protease 18 (USP18) plays an important role in regulating type I interferon (IFN) signaling in innate immunity, and has a crucial impact on the IFN therapeutic effect. Although significant progress has been made in elucidating USP18 function in mammals, the role of USP18 in ducks (duUSP18) remains poorly understood. In this study, we cloned the USP18 gene from white crested ducks by reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of complementary DNA (cDNA) ends. We determined that duUSP18 cDNA contains a 52-bp 5'UTR, a 1,131-bp open reading frame and a 356-bp 3'UTR, and encodes a 376-amino acid protein. Multiple sequence alignments showed that duUSP18 shares high similarity with USP18 from other vertebrates. Overexpression of duUSP18 inhibited nuclear factor-κB (NF-κB) and interferon regulatory factor 1 (IRF1) activity, and reduced IFN-β production following 5' triphosphate double-stranded RNA (5'ppp dsRNA) or lipopolysaccharide (LPS) stimulation. duUSP18 knockdown significantly activated 5'ppp dsRNA-induced and LPS-induced NF-κB and IRF1 activation, and induced IFN-β expression in duck embryo fibroblasts. Furthermore, Quantitative real-time PCR (qRT-PCR) revealed that overexpression or knockdown of duUSP18 could alter the expression of genes related to the RLR-mediated IFN signaling pathway following the treatment with 5'ppp dsRNA. In addition, site-directed mutation analysis revealed that cysteine 66 (C66), histidine 313 (H313), and histidine 321 (H321) of duUSP18 were critical for inhibiting IFN-β activity. Taken together, these results suggest that duck USP18 plays an important role in innate immune responses against double-stranded RNA viruses in the RLR-mediated IFN signaling pathway, and that further studies are warranted to elucidate its underlying mechanisms, which could provide molecular insights into the effect of the treatment of duck diseases.

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Expression characterization, genomic structure and function analysis of fish ubiquitin-specific protease 18 (USP18) genes

Cited by 12 publications

References 48 publications

Distinct herpesvirus resistances and immune responses of three gynogenetic clones of gibel carp revealed by comprehensive transcriptomes

Distinct herpesvirus resistances and immune responses of three gynogenetic clones of gibel carp revealed by comprehensive transcriptomes

Bioinformatics analysis of the molecular mechanism underlying Huntington's disease

Negative regulation of the RLR‐mediated IFN signaling pathway by duck ubiquitin‐specific protease 18 (USP18)

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