HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish
•ΔhupA mutant was found to be defective in cell growth, H2S production, and acid adaptation in log phase cultures.•ΔhupA mutant up-regulated the transcription levels of recA and sulA, resulting in filamentous morphology.•ΔhupA mutant showed a striking defect in EPC cell invasion, and the adhesion an...
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creator | Wang, Limei Xiao, Jingfan Cui, Shilei Wang, Qiyao Wu, Haizhen Liu, Qin Zhang, Yuanxing |
description | •ΔhupA mutant was found to be defective in cell growth, H2S production, and acid adaptation in log phase cultures.•ΔhupA mutant up-regulated the transcription levels of recA and sulA, resulting in filamentous morphology.•ΔhupA mutant showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures.•ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish.
Edwardsiella tarda is a rod-shaped Gram-negative pathogenic bacterium that causes hemorrhagic septicemia in fish. Nucleoid-associated protein HU is a basic DNA-binding protein with structural specificity in regulating genes expression. In wild-type E. tarda EIB202, HU is composed of two subunits HUα (hupA) and HUβ (hupB), and exists in homodimer or heterodimer forms. Different from the wild-type and ΔhupB mutant, ΔhupA mutant was found to be defective in cell growth, H2S production, acid adaptation, and exhibited abnormal cell division resulting in a filamentous phenotype in log phase bacteria. The qRT-PCR result showed that deletion of hupA significantly up-regulated the transcription levels of recA and sulA, which in turn stimulated RecA-dependent pathway to prevent cell division, resulting in filamentous morphology in E. tarda. Furthermore, the elongated ΔhupA cells showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures. Confocal laser scanning microscopy revealed that filamentous bacteria failed to adhere to and could not be internalized into EPC. When some of the bacteria regained the rod-shape morphology in stationary cultures, the ΔhupA mutants showed increased adhesion and internalization rates into EPC. Moreover, ΔhupA mutant exhibited delayed mortalities (for two days) in zebrafish but the LD50 increased 17 folds. Immunohistochemical analysis showed that ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish. This study indicates that HU protein and strains morphology play essential roles in the virulence network of E. tarda. |
doi_str_mv | 10.1016/j.vetmic.2014.03.030 |
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Edwardsiella tarda is a rod-shaped Gram-negative pathogenic bacterium that causes hemorrhagic septicemia in fish. Nucleoid-associated protein HU is a basic DNA-binding protein with structural specificity in regulating genes expression. In wild-type E. tarda EIB202, HU is composed of two subunits HUα (hupA) and HUβ (hupB), and exists in homodimer or heterodimer forms. Different from the wild-type and ΔhupB mutant, ΔhupA mutant was found to be defective in cell growth, H2S production, acid adaptation, and exhibited abnormal cell division resulting in a filamentous phenotype in log phase bacteria. The qRT-PCR result showed that deletion of hupA significantly up-regulated the transcription levels of recA and sulA, which in turn stimulated RecA-dependent pathway to prevent cell division, resulting in filamentous morphology in E. tarda. Furthermore, the elongated ΔhupA cells showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures. Confocal laser scanning microscopy revealed that filamentous bacteria failed to adhere to and could not be internalized into EPC. When some of the bacteria regained the rod-shape morphology in stationary cultures, the ΔhupA mutants showed increased adhesion and internalization rates into EPC. Moreover, ΔhupA mutant exhibited delayed mortalities (for two days) in zebrafish but the LD50 increased 17 folds. Immunohistochemical analysis showed that ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish. This study indicates that HU protein and strains morphology play essential roles in the virulence network of E. tarda.</description><identifier>ISSN: 0378-1135</identifier><identifier>EISSN: 1873-2542</identifier><identifier>DOI: 10.1016/j.vetmic.2014.03.030</identifier><identifier>PMID: 24793099</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Bacterial Outer Membrane Proteins - genetics ; Bacterial Outer Membrane Proteins - metabolism ; Bacterial Proteins - genetics ; Bacterial Proteins - metabolism ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Danio rerio ; Edwardsiella tarda ; Edwardsiella tarda - genetics ; Edwardsiella tarda - pathogenicity ; Enterobacteriaceae Infections - microbiology ; Enterobacteriaceae Infections - mortality ; Enterobacteriaceae Infections - veterinary ; Filamentation ; Fish Diseases - microbiology ; Fish Diseases - mortality ; Freshwater ; Mutation ; Nucleoid-associated protein ; Sequence Deletion ; Up-Regulation ; Virulence ; Virulence - genetics ; Zebrafish - microbiology</subject><ispartof>Veterinary microbiology, 2014-06, Vol.171 (1-2), p.165-174</ispartof><rights>2014 Elsevier B.V.</rights><rights>Copyright © 2014 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-ad58e08c17827b7f8adf51ddb5baf7bf90e81bb8b88784d325c1f9ede01ee0453</citedby><cites>FETCH-LOGICAL-c461t-ad58e08c17827b7f8adf51ddb5baf7bf90e81bb8b88784d325c1f9ede01ee0453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.vetmic.2014.03.030$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24793099$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Limei</creatorcontrib><creatorcontrib>Xiao, Jingfan</creatorcontrib><creatorcontrib>Cui, Shilei</creatorcontrib><creatorcontrib>Wang, Qiyao</creatorcontrib><creatorcontrib>Wu, Haizhen</creatorcontrib><creatorcontrib>Liu, Qin</creatorcontrib><creatorcontrib>Zhang, Yuanxing</creatorcontrib><title>HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish</title><title>Veterinary microbiology</title><addtitle>Vet Microbiol</addtitle><description>•ΔhupA mutant was found to be defective in cell growth, H2S production, and acid adaptation in log phase cultures.•ΔhupA mutant up-regulated the transcription levels of recA and sulA, resulting in filamentous morphology.•ΔhupA mutant showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures.•ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish.
Edwardsiella tarda is a rod-shaped Gram-negative pathogenic bacterium that causes hemorrhagic septicemia in fish. Nucleoid-associated protein HU is a basic DNA-binding protein with structural specificity in regulating genes expression. In wild-type E. tarda EIB202, HU is composed of two subunits HUα (hupA) and HUβ (hupB), and exists in homodimer or heterodimer forms. Different from the wild-type and ΔhupB mutant, ΔhupA mutant was found to be defective in cell growth, H2S production, acid adaptation, and exhibited abnormal cell division resulting in a filamentous phenotype in log phase bacteria. The qRT-PCR result showed that deletion of hupA significantly up-regulated the transcription levels of recA and sulA, which in turn stimulated RecA-dependent pathway to prevent cell division, resulting in filamentous morphology in E. tarda. Furthermore, the elongated ΔhupA cells showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures. Confocal laser scanning microscopy revealed that filamentous bacteria failed to adhere to and could not be internalized into EPC. When some of the bacteria regained the rod-shape morphology in stationary cultures, the ΔhupA mutants showed increased adhesion and internalization rates into EPC. Moreover, ΔhupA mutant exhibited delayed mortalities (for two days) in zebrafish but the LD50 increased 17 folds. Immunohistochemical analysis showed that ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish. This study indicates that HU protein and strains morphology play essential roles in the virulence network of E. tarda.</description><subject>Animals</subject><subject>Bacterial Outer Membrane Proteins - genetics</subject><subject>Bacterial Outer Membrane Proteins - metabolism</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - metabolism</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Danio rerio</subject><subject>Edwardsiella tarda</subject><subject>Edwardsiella tarda - genetics</subject><subject>Edwardsiella tarda - pathogenicity</subject><subject>Enterobacteriaceae Infections - microbiology</subject><subject>Enterobacteriaceae Infections - mortality</subject><subject>Enterobacteriaceae Infections - veterinary</subject><subject>Filamentation</subject><subject>Fish Diseases - microbiology</subject><subject>Fish Diseases - mortality</subject><subject>Freshwater</subject><subject>Mutation</subject><subject>Nucleoid-associated protein</subject><subject>Sequence Deletion</subject><subject>Up-Regulation</subject><subject>Virulence</subject><subject>Virulence - genetics</subject><subject>Zebrafish - microbiology</subject><issn>0378-1135</issn><issn>1873-2542</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU-L1TAUxYMoznP0G4hk6abPmyZ5STeCDKMjDLhx1iF_bufl0aY1aZ_MrPzotnR0KcKFhPA7597cQ8hbBnsG7PDhtD_j1Ee_r4GJPfCl4BnZMa14VUtRPyc74EpXjHF5QV6VcgIA0RzgJbmohWo4NM2O_Lq5q2IKs8dAx6F76Ic8Hoe50DZ2tsc02SkOica0PJQjHe10HO4x0evw0-ZQInadpdNytbRDG2K6p9NAM26OMZ1tWfU2BXqOee4weVzdHtFlu1q-Ji9a2xV883RekrvP19-vbqrbb1--Xn26rbw4sKmyQWoE7ZnStXKq1Ta0koXgpLOtcm0DqJlz2mmttAi8lp61DQYEhghC8kvyfvMd8_BjxjKZPha_jp9w-a9hUkDND1yq_0BrwRSTDSyo2FCfh1IytmbMsbf5wTAwa0zmZLaYzBqTAb7UKnv31GF2PYa_oj-5LMDHDcBlJeeI2RQf192FmNFPJgzx3x1-A-MGqKI</recordid><startdate>20140625</startdate><enddate>20140625</enddate><creator>Wang, Limei</creator><creator>Xiao, Jingfan</creator><creator>Cui, Shilei</creator><creator>Wang, Qiyao</creator><creator>Wu, Haizhen</creator><creator>Liu, Qin</creator><creator>Zhang, Yuanxing</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QL</scope><scope>C1K</scope><scope>F1W</scope><scope>H95</scope><scope>H98</scope><scope>L.G</scope></search><sort><creationdate>20140625</creationdate><title>HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish</title><author>Wang, Limei ; Xiao, Jingfan ; Cui, Shilei ; Wang, Qiyao ; Wu, Haizhen ; Liu, Qin ; Zhang, Yuanxing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-ad58e08c17827b7f8adf51ddb5baf7bf90e81bb8b88784d325c1f9ede01ee0453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Bacterial Outer Membrane Proteins - genetics</topic><topic>Bacterial Outer Membrane Proteins - metabolism</topic><topic>Bacterial Proteins - genetics</topic><topic>Bacterial Proteins - metabolism</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Danio rerio</topic><topic>Edwardsiella tarda</topic><topic>Edwardsiella tarda - genetics</topic><topic>Edwardsiella tarda - pathogenicity</topic><topic>Enterobacteriaceae Infections - microbiology</topic><topic>Enterobacteriaceae Infections - mortality</topic><topic>Enterobacteriaceae Infections - veterinary</topic><topic>Filamentation</topic><topic>Fish Diseases - microbiology</topic><topic>Fish Diseases - mortality</topic><topic>Freshwater</topic><topic>Mutation</topic><topic>Nucleoid-associated protein</topic><topic>Sequence Deletion</topic><topic>Up-Regulation</topic><topic>Virulence</topic><topic>Virulence - genetics</topic><topic>Zebrafish - microbiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Limei</creatorcontrib><creatorcontrib>Xiao, Jingfan</creatorcontrib><creatorcontrib>Cui, Shilei</creatorcontrib><creatorcontrib>Wang, Qiyao</creatorcontrib><creatorcontrib>Wu, Haizhen</creatorcontrib><creatorcontrib>Liu, Qin</creatorcontrib><creatorcontrib>Zhang, Yuanxing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Aquaculture Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><jtitle>Veterinary microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Limei</au><au>Xiao, Jingfan</au><au>Cui, Shilei</au><au>Wang, Qiyao</au><au>Wu, Haizhen</au><au>Liu, Qin</au><au>Zhang, Yuanxing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish</atitle><jtitle>Veterinary microbiology</jtitle><addtitle>Vet Microbiol</addtitle><date>2014-06-25</date><risdate>2014</risdate><volume>171</volume><issue>1-2</issue><spage>165</spage><epage>174</epage><pages>165-174</pages><issn>0378-1135</issn><eissn>1873-2542</eissn><abstract>•ΔhupA mutant was found to be defective in cell growth, H2S production, and acid adaptation in log phase cultures.•ΔhupA mutant up-regulated the transcription levels of recA and sulA, resulting in filamentous morphology.•ΔhupA mutant showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures.•ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish.
Edwardsiella tarda is a rod-shaped Gram-negative pathogenic bacterium that causes hemorrhagic septicemia in fish. Nucleoid-associated protein HU is a basic DNA-binding protein with structural specificity in regulating genes expression. In wild-type E. tarda EIB202, HU is composed of two subunits HUα (hupA) and HUβ (hupB), and exists in homodimer or heterodimer forms. Different from the wild-type and ΔhupB mutant, ΔhupA mutant was found to be defective in cell growth, H2S production, acid adaptation, and exhibited abnormal cell division resulting in a filamentous phenotype in log phase bacteria. The qRT-PCR result showed that deletion of hupA significantly up-regulated the transcription levels of recA and sulA, which in turn stimulated RecA-dependent pathway to prevent cell division, resulting in filamentous morphology in E. tarda. Furthermore, the elongated ΔhupA cells showed a striking defect in EPC cell invasion, and the adhesion and internalization rates were reduced to 25% and 27% of the wild-type in log phase cultures. Confocal laser scanning microscopy revealed that filamentous bacteria failed to adhere to and could not be internalized into EPC. When some of the bacteria regained the rod-shape morphology in stationary cultures, the ΔhupA mutants showed increased adhesion and internalization rates into EPC. Moreover, ΔhupA mutant exhibited delayed mortalities (for two days) in zebrafish but the LD50 increased 17 folds. Immunohistochemical analysis showed that ΔhupA mutant reduced proliferation abilities in the muscle, liver and intestine of zebrafish. This study indicates that HU protein and strains morphology play essential roles in the virulence network of E. tarda.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>24793099</pmid><doi>10.1016/j.vetmic.2014.03.030</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Bacterial Outer Membrane Proteins - genetics Bacterial Outer Membrane Proteins - metabolism Bacterial Proteins - genetics Bacterial Proteins - metabolism Carrier Proteins - genetics Carrier Proteins - metabolism Danio rerio Edwardsiella tarda Edwardsiella tarda - genetics Edwardsiella tarda - pathogenicity Enterobacteriaceae Infections - microbiology Enterobacteriaceae Infections - mortality Enterobacteriaceae Infections - veterinary Filamentation Fish Diseases - microbiology Fish Diseases - mortality Freshwater Mutation Nucleoid-associated protein Sequence Deletion Up-Regulation Virulence Virulence - genetics Zebrafish - microbiology |
title | HU-induced polymorphous filamentation in fish pathogen Edwardsiella tarda leading to reduced invasion and virulence in zebrafish |
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