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Acute hepatopancreatic necrosis disease (AHPND) caused by PirABVP-producing strain of Vibrio parahaemolyticus, VPAHPND, has seriously impacted the shrimp production. Although the VPAHPND toxin is known as the VPAHPND virulence factor, a receptor that mediates its action has not been identified. An in-house transcriptome of Litopenaeus vannamei hemocytes allows us to identify two proteins from the aminopeptidase N family, LvAPN1 and LvAPN2, the proteins of which in insect are known to be receptors for Cry toxin. The membrane-bound APN, LvAPN1, was characterized to determine if it was a VPAHPND toxin receptor. The increased expression of LvAPN1 was found in hemocytes, stomach, and hepatopancreas after the shrimp were challenged with either VPAHPND or the partially purified VPAHPND toxin. LvAPN1 knockdown reduced the mortality, histopathological signs of AHPND in the hepatopancreas, and the number of virulent VPAHPND bacteria in the stomach after VPAHPND toxin challenge. In addition, LvAPN1 silencing prevented the toxin from causing severe damage to the hemocytes and sustained both the total hemocyte count (THC) and the percentage of living hemocytes. We found that the rLvAPN1 directly bound to both rPirAVP and rPirBVP toxins, supporting the notion that silencing of LvAPN1 prevented the VPAHPND toxin from passing through the cell membrane of hemocytes. We concluded that the LvAPN1 was involved in AHPND pathogenesis and acted as a VPAHPND toxin receptor mediating the toxin penetration into hemocytes. Besides, this was the first report on the toxic effect of VPAHPND toxin on hemocytes other than the known target tissues, hepatopancreas and stomach.
Waruntorn Luangtrakul; Pakpoom Boonchuen; Phattarunda Jaree; Ramya Kumar; Han-Ching Wang; Kunlaya Somboonwiwat. Cytotoxicity of Vibrio parahaemolyticus AHPND toxin on shrimp hemocytes, a newly identified target tissue, involves binding of toxin to aminopeptidase N1 receptor. PLOS Pathogens 2021, 17, e1009463 .
AMA StyleWaruntorn Luangtrakul, Pakpoom Boonchuen, Phattarunda Jaree, Ramya Kumar, Han-Ching Wang, Kunlaya Somboonwiwat. Cytotoxicity of Vibrio parahaemolyticus AHPND toxin on shrimp hemocytes, a newly identified target tissue, involves binding of toxin to aminopeptidase N1 receptor. PLOS Pathogens. 2021; 17 (3):e1009463.
Chicago/Turabian StyleWaruntorn Luangtrakul; Pakpoom Boonchuen; Phattarunda Jaree; Ramya Kumar; Han-Ching Wang; Kunlaya Somboonwiwat. 2021. "Cytotoxicity of Vibrio parahaemolyticus AHPND toxin on shrimp hemocytes, a newly identified target tissue, involves binding of toxin to aminopeptidase N1 receptor." PLOS Pathogens 17, no. 3: e1009463.
Recently, l-amino acid oxidases (LAAOs) have been identified in several fish species as first-line defense molecules against bacterial infection. Here, we report the cloning and characterization of a fish LAAO gene, EcLAAO2, from orange-spotted grouper (Epinephelus coioides). The full-length cDNA is 3030 bp, with an ORF encoding a protein of 511 amino acids. EcLAAO2 is mainly expressed in the fin, gill, and intestine. Its expression is upregulated in several immune organs after challenge with lipopolysaccharide (LPS) and poly (I:C). The recombinant EcLAAO2 protein (rEcLAAO2), expressed and purified from a baculovirus expression system, was determined to be a glycosylated dimer. According to a hydrogen peroxide-production assay, the recombinant protein was identified as having LAAO enzyme activity with substrate preference for L-Phe and L-Trp, but not L-Lys as other known fish LAAOs. rEcLAAO2 could effectively inhibit the growth of Vibrio parahaemolyticus, Staphylococcus aureus, and Bacillus subtilis while exhibiting less effective inhibition of the growth of Escherichia coli. Finally, protein models based on sequence homology were constructed to predict the three-dimensional structure of EcLAAO2 as well as to explain the difference in substrate specificity between EcLAAO2 and other reported fish LAAOs. In conclusion, this study identifies EcLAAO2 as a novel fish LAAO with a substrate preference distinct from other known fish LAAOs and reveals that it may function against invading pathogens.
Jiann-Horng Leu; Chi-Hang Tsai; Chia-Hsun Yang; Hsin-Yiu Chou; Hao-Ching Wang. Identification and characterization of l-amino acid oxidase 2 gene in orange-spotted grouper (Epinephelus coioides). Developmental & Comparative Immunology 2021, 120, 104058 .
AMA StyleJiann-Horng Leu, Chi-Hang Tsai, Chia-Hsun Yang, Hsin-Yiu Chou, Hao-Ching Wang. Identification and characterization of l-amino acid oxidase 2 gene in orange-spotted grouper (Epinephelus coioides). Developmental & Comparative Immunology. 2021; 120 ():104058.
Chicago/Turabian StyleJiann-Horng Leu; Chi-Hang Tsai; Chia-Hsun Yang; Hsin-Yiu Chou; Hao-Ching Wang. 2021. "Identification and characterization of l-amino acid oxidase 2 gene in orange-spotted grouper (Epinephelus coioides)." Developmental & Comparative Immunology 120, no. : 104058.
Acute hepatopancreatic necrosis disease (AHPND) is a lethal shrimp disease. The pathogenic agent of this disease is a special Vibrio parahaemolyticus strain that contains a pVA1 plasmid. The protein products of two toxin genes in pVA1, pirAvp and pirBvp, targeted the shrimp’s hepatopancreatic cells and were identified as the major virulence factors. However, in addition to pirAvp and pirBvp, pVA1 also contains about ~90 other open-reading frames (ORFs), which may encode functional proteins. NCBI BLASTp annotations of the functional roles of 40 pVA1 genes reveal transposases, conjugation factors, and antirestriction proteins that are involved in horizontal gene transfer, plasmid transmission, and maintenance, as well as components of type II and III secretion systems that may facilitate the toxic effects of pVA1-containing Vibrio spp. There is also evidence of a post-segregational killing (PSK) system that would ensure that only pVA1 plasmid-containing bacteria could survive after segregation. Here, in this review, we assess the functional importance of these pVA1 genes and consider those which might be worthy of further study.
Hao-Ching Wang; Shin-Jen Lin; Arpita Mohapatra; Ramya Kumar; Han-Ching Wang. A Review of the Functional Annotations of Important Genes in the AHPND-Causing pVA1 Plasmid. Microorganisms 2020, 8, 996 .
AMA StyleHao-Ching Wang, Shin-Jen Lin, Arpita Mohapatra, Ramya Kumar, Han-Ching Wang. A Review of the Functional Annotations of Important Genes in the AHPND-Causing pVA1 Plasmid. Microorganisms. 2020; 8 (7):996.
Chicago/Turabian StyleHao-Ching Wang; Shin-Jen Lin; Arpita Mohapatra; Ramya Kumar; Han-Ching Wang. 2020. "A Review of the Functional Annotations of Important Genes in the AHPND-Causing pVA1 Plasmid." Microorganisms 8, no. 7: 996.
Uracil-DNA glycosylases (UDGs) are conserved DNA-repair enzymes that can be found in many species, including herpesviruses. Since they play crucial roles for efficient viral DNA replication in herpesviruses, they have been considered as potential antiviral targets. In our previous work, Staphylococcus aureus SAUGI was identified as a DNA mimic protein that targets UDGs from S. aureus, human, Herpes simplex virus (HSV) and Epstein-Barr virus (EBV). Interestingly, SAUGI has the strongest inhibitory effects with EBVUDG. Here, we determined complex structures of SAUGI with EBVUDG and another γ-herpesvirus UDG from Kaposi's sarcoma-associated herpesvirus (KSHVUDG), which SAUGI fails to effectively inhibit. Structural analysis of the SAUGI/EBVUDG complex suggests that the additional interaction between SAUGI and the leucine loop may explain why SAUGI shows the highest binding capacity with EBVUDG. In contrast, SAUGI appears to make only partial contacts with the key components responsible for the compression and stabilization of the DNA backbone in the leucine loop extension of KSHVUDG. The findings in this study provide a molecular explanation for the differential inhibitory effects and binding strengths that SAUGI has on these two UDGs, and the structural basis of the differences should be helpful in developing inhibitors that would interfere with viral DNA replication.
Yi-Ting Liao; Shin-Jen Lin; Tzu-Ping Ko; Chang-Yi Liu; Kai-Cheng Hsu; Hao-Ching Wang. Structural insight into the differential interactions between the DNA mimic protein SAUGI and two gamma herpesvirus uracil-DNA glycosylases. International Journal of Biological Macromolecules 2020, 160, 903 -914.
AMA StyleYi-Ting Liao, Shin-Jen Lin, Tzu-Ping Ko, Chang-Yi Liu, Kai-Cheng Hsu, Hao-Ching Wang. Structural insight into the differential interactions between the DNA mimic protein SAUGI and two gamma herpesvirus uracil-DNA glycosylases. International Journal of Biological Macromolecules. 2020; 160 ():903-914.
Chicago/Turabian StyleYi-Ting Liao; Shin-Jen Lin; Tzu-Ping Ko; Chang-Yi Liu; Kai-Cheng Hsu; Hao-Ching Wang. 2020. "Structural insight into the differential interactions between the DNA mimic protein SAUGI and two gamma herpesvirus uracil-DNA glycosylases." International Journal of Biological Macromolecules 160, no. : 903-914.
Asian countries are the major producers of cultured Penaeid shrimps such as Penaeus monodon and Penaeus (Litopenaeus) vannamei. In recent years, shrimp production has declined due to the emergence of a bacterial disease called acute hepatopancreatic necrosis disease (AHPND). This disease is mainly caused by Vibrio parahaemolyticus, but other Vibrio species are also known to cause AHPND in shrimps. Here, in addition to reviewing recent developments in the field of AHPND diagnosis, host responses to AHPND, the role of microbiota during AHPND infection and the current treatment options for AHPND, we also describe a model of AHPND pathogenesis.
Ramya Kumar; Tze Hann Ng; Han-Ching Wang. Acute hepatopancreatic necrosis disease in penaeid shrimp. Reviews in Aquaculture 2020, 12, 1 .
AMA StyleRamya Kumar, Tze Hann Ng, Han-Ching Wang. Acute hepatopancreatic necrosis disease in penaeid shrimp. Reviews in Aquaculture. 2020; 12 (3):1.
Chicago/Turabian StyleRamya Kumar; Tze Hann Ng; Han-Ching Wang. 2020. "Acute hepatopancreatic necrosis disease in penaeid shrimp." Reviews in Aquaculture 12, no. 3: 1.
Acute hepatopancreatic necrosis disease (AHPND) is a recently emerged disease in aqua cultured shrimp that is caused by virulent strains of Vibrio parahaemolyticus (VP). Our previous study used transcriptomics to identify key pathogenic factors in the stomach of AHPND-infected shrimp (Litopenaeus vannamei), and here we used a different subset of the same data to construct a gene-to-gene expression correlation network to identify immune-responsive genes. LvSerpin7 was found to have the highest number of correlations after infection, and it also showed a significant increase in mRNA expression. LvSerpin7 is expressed in all tissues but its expression levels are highest in hemocytes. After successfully silencing LvSerpin7 transcript prior to AHPND challenge, mortality was significantly increased relative to the controls and reached 100% within 36 h post infection. Compared to the controls, the phenoloxidase (PO) activity also increased in both hemolymph and stomach. Recombinant LvSerpin7 inhibited shrimp PO activity in vitro, and we also found that rLvSerpin7 inhibited the growth of AHPND-causing bacteria. These results suggest that LvSerpin7 might reduce the toxic effects that result from unregulated activation of the PO defense system by AHPND-causing bacteria.
Kantamas Apitanyasai; Che-Chih Chang; Tze Hann Ng; Yen Siong Ng; Jiun-Hung Liou; Chu-Fang Lo; Shih-Shun Lin; Han-Ching Wang. Penaeus vannamei serine proteinase inhibitor 7 (LvSerpin7) acts as an immune brake by regulating the proPO system in AHPND-affected shrimp. Developmental & Comparative Immunology 2019, 106, 103600 .
AMA StyleKantamas Apitanyasai, Che-Chih Chang, Tze Hann Ng, Yen Siong Ng, Jiun-Hung Liou, Chu-Fang Lo, Shih-Shun Lin, Han-Ching Wang. Penaeus vannamei serine proteinase inhibitor 7 (LvSerpin7) acts as an immune brake by regulating the proPO system in AHPND-affected shrimp. Developmental & Comparative Immunology. 2019; 106 ():103600.
Chicago/Turabian StyleKantamas Apitanyasai; Che-Chih Chang; Tze Hann Ng; Yen Siong Ng; Jiun-Hung Liou; Chu-Fang Lo; Shih-Shun Lin; Han-Ching Wang. 2019. "Penaeus vannamei serine proteinase inhibitor 7 (LvSerpin7) acts as an immune brake by regulating the proPO system in AHPND-affected shrimp." Developmental & Comparative Immunology 106, no. : 103600.
Using two advanced sequencing approaches, Illumina and PacBio, we derive the entire Dscam gene from an M2 assembly of the complete Penaeus monodon genome. The P. monodon Dscam (PmDscam) gene is ~266 kbp, with a total of 44 exons, 5 of which are subject to alternative splicing. PmDscam has a conserved architectural structure consisting of an extracellular region with hypervariable Ig domains, a transmembrane domain, and a cytoplasmic tail. We show that, contrary to a previous report, there are in fact 26, 81 and 26 alternative exons in N-terminal Ig2, N-terminal Ig3 and the entirety of Ig7, respectively. We also identified two alternatively spliced exons in the cytoplasmic tail, with transmembrane domains in exon variants 32.1 and 32.2, and stop codons in exon variants 44.1 and 44.2. This means that alternative splicing is involved in the selection of the stop codon. There are also 7 non-constitutive cytoplasmic tail exons that can either be included or skipped. Alternative splicing and the non-constitutive exons together produce more than 21 million isoform combinations from one PmDscam locus in the P. monodon gene. A public-facing database that allows BLAST searches of all 175 exons in the PmDscam gene has been established at http://pmdscam.dbbs.ncku.edu.tw/.
Kantamas Apitanyasai; Shiao-Wei Huang; Tze Hann Ng; Shu-Ting He; Yu-Hsun Huang; Shen-Po Chiu; Kuan-Chien Tseng; Shih-Shun Lin; Wen-Chi Chang; James G. Baldwin-Brown; Anthony D. Long; Chu-Fang Lo; Hon-Tsen Yu; Han-Ching Wang. The gene structure and hypervariability of the complete Penaeus monodon Dscam gene. Scientific Reports 2019, 9, 16595 .
AMA StyleKantamas Apitanyasai, Shiao-Wei Huang, Tze Hann Ng, Shu-Ting He, Yu-Hsun Huang, Shen-Po Chiu, Kuan-Chien Tseng, Shih-Shun Lin, Wen-Chi Chang, James G. Baldwin-Brown, Anthony D. Long, Chu-Fang Lo, Hon-Tsen Yu, Han-Ching Wang. The gene structure and hypervariability of the complete Penaeus monodon Dscam gene. Scientific Reports. 2019; 9 (1):16595.
Chicago/Turabian StyleKantamas Apitanyasai; Shiao-Wei Huang; Tze Hann Ng; Shu-Ting He; Yu-Hsun Huang; Shen-Po Chiu; Kuan-Chien Tseng; Shih-Shun Lin; Wen-Chi Chang; James G. Baldwin-Brown; Anthony D. Long; Chu-Fang Lo; Hon-Tsen Yu; Han-Ching Wang. 2019. "The gene structure and hypervariability of the complete Penaeus monodon Dscam gene." Scientific Reports 9, no. 1: 16595.
Acute hepatopancreas necrosis disease is a recently emerged shrimp disease that is caused by virulent strains of V. parahaemolyticus. Although AHPND poses a serious threat to the shrimp industry, particularly in Asia, its underlying pathogenic mechanisms are not well characterized. Since a previous transcriptomic study showed upregulation of the apical sodium bile acid transporter (LvASBT), our objective here was to explore the role of bile acids and bile acid transporters in AHPND infection. We confirmed that mRNA expression of LvASBT was upregulated in the stomach of AHPND‐infected shrimps. Bile acid concentrations were also higher in the stomach of AHPND‐infected shrimp and correlated with high expression of pVA plasmid and Pir toxins. In vitro assays showed that bile acids enhanced biofilm formation and increased the release of PirABvp toxins in AHPND‐causing V. parahaemolyticus, while in vivo inhibition of LvASBT by GSK2330672 reduced the copy numbers of pVA plasmid, Pir toxin and reduced the amounts of bile acids in AHPND‐infected shrimp stomach. Transcriptomics data for AHPND‐causing V. parahaemolyticus treated with bile acids showed upregulation of various genes involved in membrane transport, RND efflux pumps and a bacterial secretion system. Taken together, our results show that AHPND‐causing V. parahaemolyticus virulence is positively regulated by bile acids and that LvASBT and bile acids in shrimp stomach have important roles in AHPND pathogenesis.
Ramya Kumar; Tze Hann Ng; Che‐Chih Chang; Teng‐Chun Tung; Shih‐Shun Lin; Chu‐Fang Lo; Han‐Ching Wang. Bile acid and bile acid transporters are involved in the pathogenesis of acute hepatopancreatic necrosis disease in white shrimpLitopenaeus vannamei. Cellular Microbiology 2019, 22, e13127 .
AMA StyleRamya Kumar, Tze Hann Ng, Che‐Chih Chang, Teng‐Chun Tung, Shih‐Shun Lin, Chu‐Fang Lo, Han‐Ching Wang. Bile acid and bile acid transporters are involved in the pathogenesis of acute hepatopancreatic necrosis disease in white shrimpLitopenaeus vannamei. Cellular Microbiology. 2019; 22 (1):e13127.
Chicago/Turabian StyleRamya Kumar; Tze Hann Ng; Che‐Chih Chang; Teng‐Chun Tung; Shih‐Shun Lin; Chu‐Fang Lo; Han‐Ching Wang. 2019. "Bile acid and bile acid transporters are involved in the pathogenesis of acute hepatopancreatic necrosis disease in white shrimpLitopenaeus vannamei." Cellular Microbiology 22, no. 1: e13127.
Phytoplasmas are bacterial plant pathogens which can induce severe symptoms including dwarfism, phyllody and virescence in an infected plant. Because phytoplasmas infect many important crops such as peanut and papaya they have caused serious agricultural losses. The phytoplasmal effector causing phyllody 1 (PHYL1) is an important phytoplasmal pathogenic factor which affects the biological function of MADS transcription factors by interacting with their K (keratin-like) domain, thus resulting in abnormal plant developments such as phyllody. Until now, lack of information on the structure of PHYL1 has prevented a detailed understanding of the binding mechanism between PHYL1 and the MADS transcription factors. Here, we present the crystal structure of PHYL1 from peanut witches'-broom phytoplasma (PHYL1PnWB ). This protein was found to fold into a unique α-helical hairpin with exposed hydrophobic residues on its surface that may play an important role in its biological function. Using proteomics approaches, we propose a binding mode of PHYL1PnWB with the K domain of the MADS transcription factor SEPALLATA3 (SEP3_K) and identify the residues of PHYL1PnWB that are important for this interaction. Furthermore, using surface plasmon resonance we measure the binding strength of PHYL1PnWB proteins to SEP3_K. Lastly, based on confocal images, we found that α-helix 2 of PHYL1PnWB plays an important role in PHYL1-mediated degradation of SEP3. Taken together, these results provide a structural understanding of the specific binding mechanism between PHYL1PnWB and SEP3_K.
Yi‐Ting Liao; Shih‐Shun Lin; Shin‐Jen Lin; Wan‐Ting Sun; Bing‐Nan Shen; Han‐Pin Cheng; Chan‐Pin Lin; Tzu‐Ping Ko; Yi‐Fan Chen; Hao‐Ching Wang. Structural insights into the interaction between phytoplasmal effector causing phyllody 1 and MADS transcription factors. The Plant Journal 2019, 100, 706 -719.
AMA StyleYi‐Ting Liao, Shih‐Shun Lin, Shin‐Jen Lin, Wan‐Ting Sun, Bing‐Nan Shen, Han‐Pin Cheng, Chan‐Pin Lin, Tzu‐Ping Ko, Yi‐Fan Chen, Hao‐Ching Wang. Structural insights into the interaction between phytoplasmal effector causing phyllody 1 and MADS transcription factors. The Plant Journal. 2019; 100 (4):706-719.
Chicago/Turabian StyleYi‐Ting Liao; Shih‐Shun Lin; Shin‐Jen Lin; Wan‐Ting Sun; Bing‐Nan Shen; Han‐Pin Cheng; Chan‐Pin Lin; Tzu‐Ping Ko; Yi‐Fan Chen; Hao‐Ching Wang. 2019. "Structural insights into the interaction between phytoplasmal effector causing phyllody 1 and MADS transcription factors." The Plant Journal 100, no. 4: 706-719.
Vaccinia mature virus requires A26 envelope protein to mediate acid-dependent endocytosis into HeLa cells in which we hypothesized that A26 protein functions as an acid-sensitive membrane fusion suppressor. Here, we provide evidence showing that N-terminal domain (aa1-75) of A26 protein is an acid-sensitive region that regulates membrane fusion. Crystal structure of A26 protein revealed that His48 and His53 are in close contact with Lys47, Arg57, His314 and Arg312, suggesting that at low pH these His-cation pairs could initiate conformational changes through protonation of His48 and His53 and subsequent electrostatic repulsion. All the A26 mutant mature viruses that interrupted His-cation pair interactions of His48 and His 53 indeed have lost virion infectivity. Isolation of revertant viruses revealed that second site mutations caused frame shifts and premature termination of A26 protein such that reverent viruses regained cell entry through plasma membrane fusion. Together, we conclude that viral A26 protein functions as an acid-sensitive fusion suppressor during vaccinia mature virus endocytosis. Vaccinia virus is a complex large DNA virus with a large number of viral membrane proteins to facilitate cell entry. Although it is well established that vaccinia mature virus uses endocytosis to enter cells, it remains unclear how it triggers membrane fusion in the acidic environment of endosomes. Recently, we hypothesized that A26 protein in vaccinia mature virus functions as an acid-sensitive membrane fusion suppressor, which suggests a novel viral regulation not present in other enveloped viruses. We postulated that conformational changes of A26 protein at low pH result in de-repression of viral fusion complex activity to trigger viral and endosomal membrane fusion. Here, we provide structural, biochemical and biological evidence demonstrating that vaccinia A26 protein does indeed function as an acid-sensitive fusion suppressor protein to regulate vaccinia mature virus membrane fusion during endocytosis. Our data reveal an important and unique “checkpoint” for vaccinia mature virus endocytosis that has not been described for other viruses. Furthermore, by isolating adaptive vaccinia mutants that escaped endocytic blockage, we discovered that mutations within the A26L gene serve as an effective strategy for switching the viral infection route from endocytosis to plasma membrane fusion, expanding viral host range.
Hung-Wei Chang; Cheng-Han Yang; Yu-Chun Luo; Bo-Gang Su; Huei-Yin Cheng; Shu-Yun Tung; Kathleen Joyce D. Carillo; Yi-Ting Liao; Der-Lii M. Tzou; Hao-Ching Wang; Wen Chang. Vaccinia viral A26 protein is a fusion suppressor of mature virus and triggers membrane fusion through conformational change at low pH. PLOS Pathogens 2019, 15, e1007826 .
AMA StyleHung-Wei Chang, Cheng-Han Yang, Yu-Chun Luo, Bo-Gang Su, Huei-Yin Cheng, Shu-Yun Tung, Kathleen Joyce D. Carillo, Yi-Ting Liao, Der-Lii M. Tzou, Hao-Ching Wang, Wen Chang. Vaccinia viral A26 protein is a fusion suppressor of mature virus and triggers membrane fusion through conformational change at low pH. PLOS Pathogens. 2019; 15 (6):e1007826.
Chicago/Turabian StyleHung-Wei Chang; Cheng-Han Yang; Yu-Chun Luo; Bo-Gang Su; Huei-Yin Cheng; Shu-Yun Tung; Kathleen Joyce D. Carillo; Yi-Ting Liao; Der-Lii M. Tzou; Hao-Ching Wang; Wen Chang. 2019. "Vaccinia viral A26 protein is a fusion suppressor of mature virus and triggers membrane fusion through conformational change at low pH." PLOS Pathogens 15, no. 6: e1007826.
H.C. Wang; K. Apitanyasai; C.F. Lo; H.T. Yu. Complexity of Penaeus monodon Dscam gene structure occurs in both extracellular region and cytoplasmic tail. Fish & Shellfish Immunology 2019, 91, 422 .
AMA StyleH.C. Wang, K. Apitanyasai, C.F. Lo, H.T. Yu. Complexity of Penaeus monodon Dscam gene structure occurs in both extracellular region and cytoplasmic tail. Fish & Shellfish Immunology. 2019; 91 ():422.
Chicago/Turabian StyleH.C. Wang; K. Apitanyasai; C.F. Lo; H.T. Yu. 2019. "Complexity of Penaeus monodon Dscam gene structure occurs in both extracellular region and cytoplasmic tail." Fish & Shellfish Immunology 91, no. : 422.
Acute hepatopancreatic necrosis disease (AHPND) is a newly emergent penaeid shrimp disease which can cause 70–100% mortality in Penaeus vannamei and Penaeus monodon, and has resulted in enormous economic losses since its appearance. AHPND is caused by the specific strains of Vibrio parahaemolyticus that harbor the pVA1 plasmid and express PirAvp and PirBvp toxins. These two toxins have been reported to form a binary complex. When both are present, they lead to the death of shrimp epithelial cells in the hepatopancreas and cause the typical histological symptoms of AHPND. However, the binding mode of PirAvp and PirBvp has not yet been determined. Here, we used isothermal titration calorimetry (ITC) to measure the binding affinity of PirAvp and PirBvp. Since the dissociation constant (Kd = 7.33 ± 1.20 μM) was considered too low to form a sufficiently stable complex for X-ray crystallographic analysis, we used alternative methods to investigate PirAvp-PirBvp interaction, first by using gel filtration to evaluate the molecular weight of the PirAvp/PirBvp complex, and then by using cross-linking and hydrogen-deuterium exchange (HDX) mass spectrometry to further understand the interaction interface between PirAvp and PirBvp. Based on these results, we propose a heterotetrameric interaction model of this binary toxin complex. This model provides insight of how conformational changes might activate the PirBvp N-terminal pore-forming domain and should be helpful for devising effective anti-AHPND strategies in the future.
Shin-Jen Lin; Yi-Fan Chen; Kai-Cheng Hsu; Yun-Ling Chen; Tzu-Ping Ko; Chu-Fang Lo; Han-Ching Wang. Structural Insights to the Heterotetrameric Interaction between the Vibrio parahaemolyticus PirAvp and PirBvp Toxins and Activation of the Cry-Like Pore-Forming Domain. Toxins 2019, 11, 233 .
AMA StyleShin-Jen Lin, Yi-Fan Chen, Kai-Cheng Hsu, Yun-Ling Chen, Tzu-Ping Ko, Chu-Fang Lo, Han-Ching Wang. Structural Insights to the Heterotetrameric Interaction between the Vibrio parahaemolyticus PirAvp and PirBvp Toxins and Activation of the Cry-Like Pore-Forming Domain. Toxins. 2019; 11 (4):233.
Chicago/Turabian StyleShin-Jen Lin; Yi-Fan Chen; Kai-Cheng Hsu; Yun-Ling Chen; Tzu-Ping Ko; Chu-Fang Lo; Han-Ching Wang. 2019. "Structural Insights to the Heterotetrameric Interaction between the Vibrio parahaemolyticus PirAvp and PirBvp Toxins and Activation of the Cry-Like Pore-Forming Domain." Toxins 11, no. 4: 233.
For many, “DNA mimic protein” (DMP) remains an unfamiliar term. The key feature of these proteins is their DNA‐like shape and charge distribution, and they affect the activity of DNA‐binding proteins by occupying their DNA‐binding domains. Functionally, DMPs regulate mechanisms such as gene expression, restriction, and DNA repair as well as the nucleosome package. Although a few DMPs, such as phage uracil DNA glycosylase inhibitor (UGI) and overcome classical restriction (Ocr), were reported about 20 years ago, only a small number of DMPs have been studied to date. In 2014, we reviewed the functional and structural features of 16 DMPs that were known at the time. Now, seven new DMPs, namely anti‐CRISPR suppressors AcrF2, AcrF10 and AcrIIA4, human immunodeficiency virus essential factor VPR, multi‐functional inhibitor anti‐restriction nuclease (Arn), translational regulator AbbA, and putative Z‐DNA mimic MBD3, have been reported. In addition, further study of two previously known DMPs, DMP19 and SAUGI, increased our knowledge of their importance and function. Here, we discuss these updated results and address how several characteristics of the structure/sequence of DMPs (e.g. the DNA‐like charge distribution and structural D/E‐rich repeats) might someday be used to identify new DMPs using bioinformatic approach. © 2018 IUBMB Life, 2018
Hao-Ching Wang; Chia-Cheng Chou; Kai-Cheng Hsu; Chi-Hua Lee; Andrew H.-J. Wang. New paradigm of functional regulation by DNA mimic proteins: Recent updates. IUBMB Life 2018, 71, 539 -548.
AMA StyleHao-Ching Wang, Chia-Cheng Chou, Kai-Cheng Hsu, Chi-Hua Lee, Andrew H.-J. Wang. New paradigm of functional regulation by DNA mimic proteins: Recent updates. IUBMB Life. 2018; 71 (5):539-548.
Chicago/Turabian StyleHao-Ching Wang; Chia-Cheng Chou; Kai-Cheng Hsu; Chi-Hua Lee; Andrew H.-J. Wang. 2018. "New paradigm of functional regulation by DNA mimic proteins: Recent updates." IUBMB Life 71, no. 5: 539-548.
A new clade, Trichoderma formosa, secretes eliciting plant response-like 1 (Epl1), a small peptide elicitor that stimulates plant immunity. Nicotiana benthamiana pretreated with Epl1 for 3 days developed immunity against Tomato mosaic virus (ToMV) infection. The transcriptome profiles of T. formosa and N. benthamiana were obtained by deep sequencing; the transcript of Epl1 is 736 nt in length and encodes a 12-kDa peptide. Identifying critical genes in Epl1-mediated immunity was challenging due to high similarity between the transcriptome expression profiles of Epl1-treated and ToMV-infected N. benthamiana samples. Therefore, an efficient bioinformatics data mining approach was used for high-throughput transcriptomic assays in this study. We integrated gene-to-gene network analysis into the ContigViews transcriptome database, and genes related to jasmonic acid and ethylene signaling, salicylic acid signaling, leucine-rich repeats, transcription factors, and histone variants were hubs in the gene-to-gene networks. In this study, the Epl1 of T. formosa triggers plant immunity against various pathogen infections. Moreover, we demonstrated that high-throughput data mining and gene-to-gene network analysis can be used to identify critical candidate genes for further studies on the mechanisms of plant immunity.
Chi-Hua Cheng; Bing-Nan Shen; Qian-Wen Shang; Li-Yu Daisy Liu; Kou-Cheng Peng; Yan-Huey Chen; Fang-Fang Chen; Sin-Fen Hu; Yu-Tai Wang; Hao-Ching Wang; Hsin-Yi Wu; Chaur-Tsuen Lo; Shih-Shun Lin. Gene-to-Gene Network Analysis of the Mediation of Plant Innate Immunity by the Eliciting Plant Response-Like 1 (Epl1) Elicitor of Trichoderma formosa. Molecular Plant-Microbe Interactions® 2018, 31, 683 -691.
AMA StyleChi-Hua Cheng, Bing-Nan Shen, Qian-Wen Shang, Li-Yu Daisy Liu, Kou-Cheng Peng, Yan-Huey Chen, Fang-Fang Chen, Sin-Fen Hu, Yu-Tai Wang, Hao-Ching Wang, Hsin-Yi Wu, Chaur-Tsuen Lo, Shih-Shun Lin. Gene-to-Gene Network Analysis of the Mediation of Plant Innate Immunity by the Eliciting Plant Response-Like 1 (Epl1) Elicitor of Trichoderma formosa. Molecular Plant-Microbe Interactions®. 2018; 31 (7):683-691.
Chicago/Turabian StyleChi-Hua Cheng; Bing-Nan Shen; Qian-Wen Shang; Li-Yu Daisy Liu; Kou-Cheng Peng; Yan-Huey Chen; Fang-Fang Chen; Sin-Fen Hu; Yu-Tai Wang; Hao-Ching Wang; Hsin-Yi Wu; Chaur-Tsuen Lo; Shih-Shun Lin. 2018. "Gene-to-Gene Network Analysis of the Mediation of Plant Innate Immunity by the Eliciting Plant Response-Like 1 (Epl1) Elicitor of Trichoderma formosa." Molecular Plant-Microbe Interactions® 31, no. 7: 683-691.
An emerging bacterial disease, acute hepatopancreatic necrosis disease (AHPND), is caused by strains of Vibrio parahaemolyticus with an additional AHPND‐associated plasmid pVA1 encoding a virulent toxin (Pirvp) that damages the shrimp's hepatopancreas. Like other species of Vibrio, these virulent strains initially colonise the shrimp's stomach, but it is not yet understood how the bacteria or toxins are subsequently able to cross the epithelial barrier and reach the hepatopancreas. Here, by using transcriptomics and system biology methods, we investigate AHPND‐induced changes in the stomach of AHPND‐causing V. parahaemolyticus (5HP)‐infected shrimp and identify host molecular mechanisms that might explain how the integrity of the stomach barrier is compromised. We found that the expression of 376 unique genes was differentially regulated by AHPND infection. Gene ontology, protein interaction, and gene‐to‐gene correlation expression interaction analyses indicated that in addition to the immune system, a number of these genes were involved in cytoskeleton regulation by Rho GTPase. The involvement of Rho pathway regulation during AHPND pathogenesis was further supported by experiments showing that while Rho inhibitor pretreatment delayed the infection, pretreatment with Rho activator enhanced the pathogenicity of 5HP, and both the bacteria and toxin were detected sooner in the hepatopancreas. Further, disruption of the stomach epithelial structure was found in both Rho preactivated shrimp and in 5HP‐infected shrimp. Taken together, we interpret our results to mean that Rho signalling helps to mediate AHPND pathogenesis in shrimp.
Tze Hann Ng; Chia-Wei Lu; Shih-Shun Lin; Che-Chih Chang; Loc H. Tran; Wen-Chi Chang; Chu-Fang Lo; Han-Ching Wang. The Rho signalling pathway mediates the pathogenicity of AHPND‐causing V. parahaemolyticus in shrimp. Cellular Microbiology 2018, 20, e12849 .
AMA StyleTze Hann Ng, Chia-Wei Lu, Shih-Shun Lin, Che-Chih Chang, Loc H. Tran, Wen-Chi Chang, Chu-Fang Lo, Han-Ching Wang. The Rho signalling pathway mediates the pathogenicity of AHPND‐causing V. parahaemolyticus in shrimp. Cellular Microbiology. 2018; 20 (8):e12849.
Chicago/Turabian StyleTze Hann Ng; Chia-Wei Lu; Shih-Shun Lin; Che-Chih Chang; Loc H. Tran; Wen-Chi Chang; Chu-Fang Lo; Han-Ching Wang. 2018. "The Rho signalling pathway mediates the pathogenicity of AHPND‐causing V. parahaemolyticus in shrimp." Cellular Microbiology 20, no. 8: e12849.
The possibility of immunological memory in invertebrates is a topic that has recently attracted a lot of attention. Today, even vertebrates are known to exhibit innate immune responses that show memory-like properties, and since these responses are triggered by cells that are involved in the innate immune system, it seems that immune specificity and immune memory do not necessarily require the presence of B cells and T cells after all. This kind of immune response has been called "immune priming" or "trained immunity". In this report, we review recent observations and our current understanding of immunological memory within the innate immune system in cultured shrimp and crayfish after vaccination with live vaccine, killed vaccine and subunit vaccines. We also discuss the possible mechanisms involved in this immune response.
Yu-Hsuan Chang; Ramya Kumar; Tze Hann Ng; Han-Ching Wang. What vaccination studies tell us about immunological memory within the innate immune system of cultured shrimp and crayfish. Developmental & Comparative Immunology 2018, 80, 53 -66.
AMA StyleYu-Hsuan Chang, Ramya Kumar, Tze Hann Ng, Han-Ching Wang. What vaccination studies tell us about immunological memory within the innate immune system of cultured shrimp and crayfish. Developmental & Comparative Immunology. 2018; 80 ():53-66.
Chicago/Turabian StyleYu-Hsuan Chang; Ramya Kumar; Tze Hann Ng; Han-Ching Wang. 2018. "What vaccination studies tell us about immunological memory within the innate immune system of cultured shrimp and crayfish." Developmental & Comparative Immunology 80, no. : 53-66.
We report here the genome sequence of Vibrio parahaemolyticus strain M1-1, which causes a mild form of shrimp acute hepatopancreatic necrosis disease (AHPND). Compared to other virulent strains, the M1-1 genome appeared to express several additional genes, while some genes were missing. These instabilities may be related to the reduced virulence of M1-1.
Ramya Kumar; Che-Chih Chang; Tze Hann Ng; Jiun-Yan Ding; Ta-Chien Tseng; Chu-Fang Lo; Han-Ching Wang. Draft Genome Sequence of Vibrio parahaemolyticus Strain M1-1, Which Causes Acute Hepatopancreatic Necrosis Disease in Shrimp in Vietnam. Genome Announcements 2018, 6, 1 .
AMA StyleRamya Kumar, Che-Chih Chang, Tze Hann Ng, Jiun-Yan Ding, Ta-Chien Tseng, Chu-Fang Lo, Han-Ching Wang. Draft Genome Sequence of Vibrio parahaemolyticus Strain M1-1, Which Causes Acute Hepatopancreatic Necrosis Disease in Shrimp in Vietnam. Genome Announcements. 2018; 6 (3):1.
Chicago/Turabian StyleRamya Kumar; Che-Chih Chang; Tze Hann Ng; Jiun-Yan Ding; Ta-Chien Tseng; Chu-Fang Lo; Han-Ching Wang. 2018. "Draft Genome Sequence of Vibrio parahaemolyticus Strain M1-1, Which Causes Acute Hepatopancreatic Necrosis Disease in Shrimp in Vietnam." Genome Announcements 6, no. 3: 1.
DNA mimicry is a direct and effective strategy by which the mimic competes with DNA for the DNA binding sites on other proteins. Until now, only about a dozen proteins have been shown to function via this strategy, including the DNA mimic protein DMP19 from Neisseria meningitides. We have shown previously that DMP19 dimer prevents the operator DNA from binding to the transcription factor NHTF. Here, we provide new evidence that DMP19 monomer can also interact with the Neisseria nucleoid-associated protein HU. Using BS3 crosslinking, gel filtration and isothermal titration calorimetry assays, we found that DMP19 uses its monomeric form to interact with the Neisseria HU dimer. Crosslinking conjugated mass spectrometry was used to investigate the binding mode of DMP19 monomer and HU dimer. Finally, an electrophoretic mobility shift assay (EMSA) confirmed that the DNA binding affinity of HU is affected by DMP19. These results showed that DMP19 is bifunctional in the gene regulation of Neisseria through its variable oligomeric forms.
Ming-Fen Huang; Shin-Jen Lin; Tzu-Ping Ko; Yi-Ting Liao; Kai-Cheng Hsu; Hao-Ching Wang. The monomeric form of Neisseria DNA mimic protein DMP19 prevents DNA from binding to the histone-like HU protein. PLOS ONE 2017, 12, e0189461 -e0189461.
AMA StyleMing-Fen Huang, Shin-Jen Lin, Tzu-Ping Ko, Yi-Ting Liao, Kai-Cheng Hsu, Hao-Ching Wang. The monomeric form of Neisseria DNA mimic protein DMP19 prevents DNA from binding to the histone-like HU protein. PLOS ONE. 2017; 12 (12):e0189461-e0189461.
Chicago/Turabian StyleMing-Fen Huang; Shin-Jen Lin; Tzu-Ping Ko; Yi-Ting Liao; Kai-Cheng Hsu; Hao-Ching Wang. 2017. "The monomeric form of Neisseria DNA mimic protein DMP19 prevents DNA from binding to the histone-like HU protein." PLOS ONE 12, no. 12: e0189461-e0189461.
Purpose: MPT0L145 has been developed as a FGFR inhibitor exhibiting significant anti-bladder cancer activity in vitro and in vivo via promoting autophagy-dependent cell death. Here, we aim to elucidate the underlying mechanisms. Experimental Design: Autophagy flux, morphology and intracellular organelles were evaluated by western blotting, transmission electron microscope and fluorescence microscope. Molecular docking, surface plasmon resonance assay were performed to identify drug-protein interaction. Lentiviral delivery of cDNA or shRNA, and CRISPR/Cas9-mediated genome editing were used to modulate gene expression. Mitochondrial oxygen consumption rate was measured by a Seahorse XFe24 extracellular flux analyzer, and ROS level was measured by flow cytometry. Results: MPT0L145 persistently increased incomplete autophagy and phase-lucent vacuoles at the peri-nuclear region, which were identified as enlarged and alkalinized late-endosomes. Screening of a panel of lipid kinases revealed that MPT0L145 strongly inhibits PIK3C3 with a KD value of 0.53 nmol/L. Ectopic expression of PIK3C3 reversed MPT0L145-increased cell death and incomplete autophagy. Four residues (Y670, F684, I760, D761) at the ATP-binding site of PIK3C3 are important for the binding of MPT0L145. Additionally, MPT0L145 promotes mitochondrial dysfunction, ROS production and DNA damage, which may in part, contribute to cell death. ATG5-knockout rescued MPT0L145-induced cell death, suggesting simultaneous induction of autophagy is crucial to its anticancer activity. Lastly, our data demonstrated that MPT0L145 is able to overcome cisplatin resistance in bladder cancer cells. Conclusions: MPT0L145 is a first-in-class PIK3C3/FGFR inhibitor, providing an innovative strategy to design new compounds that increase autophagy, but simultaneously perturb its process to promote bladder cancer cell death.
Chun-Han Chen; Chun A. Changou; Tsung-Han Hsieh; Yu-Ching Lee; Cheng-Ying Chu; Kai-Cheng Hsu; Hao-Ching Wang; Yu-Chen Lin; Yan-Ni Lo; Yun-Ru Liu; Jing-Ping Liou; Yun Yen. Dual Inhibition of PIK3C3 and FGFR as a New Therapeutic Approach to Treat Bladder Cancer. Clinical Cancer Research 2017, 24, 1176 -1189.
AMA StyleChun-Han Chen, Chun A. Changou, Tsung-Han Hsieh, Yu-Ching Lee, Cheng-Ying Chu, Kai-Cheng Hsu, Hao-Ching Wang, Yu-Chen Lin, Yan-Ni Lo, Yun-Ru Liu, Jing-Ping Liou, Yun Yen. Dual Inhibition of PIK3C3 and FGFR as a New Therapeutic Approach to Treat Bladder Cancer. Clinical Cancer Research. 2017; 24 (5):1176-1189.
Chicago/Turabian StyleChun-Han Chen; Chun A. Changou; Tsung-Han Hsieh; Yu-Ching Lee; Cheng-Ying Chu; Kai-Cheng Hsu; Hao-Ching Wang; Yu-Chen Lin; Yan-Ni Lo; Yun-Ru Liu; Jing-Ping Liou; Yun Yen. 2017. "Dual Inhibition of PIK3C3 and FGFR as a New Therapeutic Approach to Treat Bladder Cancer." Clinical Cancer Research 24, no. 5: 1176-1189.
In aquaculture, shrimp farming is a popular field. The benefits of shrimp farming include a relatively short grow-out time, high sale price, and good cost recovery. However, outbreaks of serious diseases inflict serious losses, and acute hepatopancreatic necrosis disease (AHPND) is an emerging challenge to this industry. In South American white shrimp (Penaeus vannamei) and grass shrimp (Penaeus monodon), this disease has a 70–100% mortality. The pathogenic agent of AHPND is a specific strain of Vibrio parahaemolyticus which contains PirAvp and PirBvp toxins encoded in the pVA1 plasmid. PirAvp and PirBvp have been shown to cause the typical histological symptoms of AHPND in infected shrimps, and in this review, we will focus on our structural understanding of these toxins. By analyzing their structures, a possible cytotoxic mechanism, as well as strategies for anti-AHPND drug design, is proposed.
Shin-Jen Lin; Kai-Cheng Hsu; Hao-Ching Wang. Structural Insights into the Cytotoxic Mechanism of Vibrio parahaemolyticus PirAvp and PirBvp Toxins. Marine Drugs 2017, 15, 373 .
AMA StyleShin-Jen Lin, Kai-Cheng Hsu, Hao-Ching Wang. Structural Insights into the Cytotoxic Mechanism of Vibrio parahaemolyticus PirAvp and PirBvp Toxins. Marine Drugs. 2017; 15 (12):373.
Chicago/Turabian StyleShin-Jen Lin; Kai-Cheng Hsu; Hao-Ching Wang. 2017. "Structural Insights into the Cytotoxic Mechanism of Vibrio parahaemolyticus PirAvp and PirBvp Toxins." Marine Drugs 15, no. 12: 373.