HemN2 Regulates the Virulence of Pseudomonas donghuensis HYS through 7-Hydroxytropolone Synthesis and Oxidative Stress
Compared to pathogens and , HYS has stronger virulence towards . However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and viru...
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| Published in | Biology (Basel, Switzerland) Vol. 13; no. 6; p. 373 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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24.05.2024
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| Abstract | Compared to pathogens
and
,
HYS has stronger virulence towards
. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for
virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and
virulence were barely pursued. In this study, we hypothesized that
deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four
genes in
HYS, and we reported for the first time that deletion of
significantly reduced the virulence of HYS towards
, whereas the reduction in virulence by the other three genes was not significant. Interestingly,
deletion significantly reduced colonization of
HYS in the gut of
. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of
HYS towards
by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of
HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus
. |
|---|---|
| AbstractList | Compared to pathogens
and
,
HYS has stronger virulence towards
. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for
virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and
virulence were barely pursued. In this study, we hypothesized that
deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four
genes in
HYS, and we reported for the first time that deletion of
significantly reduced the virulence of HYS towards
, whereas the reduction in virulence by the other three genes was not significant. Interestingly,
deletion significantly reduced colonization of
HYS in the gut of
. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of
HYS towards
by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of
HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus
. Compared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying mechanisms haven’t been fully understood. The heme synthesis system is essential for Pseudomonas virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and Pseudomonas virulence were barely pursued. In this study, we hypothesized that hemN2 deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that deletion of hemN2 significantly reduced the virulence of HYS towards C. elegans, whereas the reduction in virulence by the other three genes was not significant. Interestingly, hemN2 deletion significantly reduced colonization of P. donghuensis HYS in the gut of C. elegans. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of P. donghuensis HYS towards C. elegans by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of P. donghuensis HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus Pseudomonas. Pseudomonas donghuensis HYS has lethal virulence towards Caenorhabditis elegans. Anaerobic coproporphyrinogen III oxidase (HemN) is involved in Pseudomonas heme synthesis. However, no research thus far has examined the contribution of HemN to the virulence of Pseudomonas. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that the deletion of the hemN2 gene significantly reduced the virulence of P. donghuensis HYS towards C. elegans. HemN2 was negatively regulated by the Gac system and regulated bacterial virulence via 7-hydroxytropolone (7-HT) synthesis and redox levels. Our findings revealed the key role of HemN2 in bacterial virulence, which may help us to better understand the strong pathogenicity of the genus Pseudomonas. Compared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for Pseudomonas virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and Pseudomonas virulence were barely pursued. In this study, we hypothesized that hemN2 deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that deletion of hemN2 significantly reduced the virulence of HYS towards C. elegans, whereas the reduction in virulence by the other three genes was not significant. Interestingly, hemN2 deletion significantly reduced colonization of P. donghuensis HYS in the gut of C. elegans. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of P. donghuensis HYS towards C. elegans by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of P. donghuensis HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus Pseudomonas.Compared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for Pseudomonas virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and Pseudomonas virulence were barely pursued. In this study, we hypothesized that hemN2 deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that deletion of hemN2 significantly reduced the virulence of HYS towards C. elegans, whereas the reduction in virulence by the other three genes was not significant. Interestingly, hemN2 deletion significantly reduced colonization of P. donghuensis HYS in the gut of C. elegans. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of P. donghuensis HYS towards C. elegans by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of P. donghuensis HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus Pseudomonas. Pseudomonas donghuensis HYS has lethal virulence towards Caenorhabditis elegans. Anaerobic coproporphyrinogen III oxidase (HemN) is involved in Pseudomonas heme synthesis. However, no research thus far has examined the contribution of HemN to the virulence of Pseudomonas. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that the deletion of the hemN2 gene significantly reduced the virulence of P. donghuensis HYS towards C. elegans. HemN2 was negatively regulated by the Gac system and regulated bacterial virulence via 7-hydroxytropolone (7-HT) synthesis and redox levels. Our findings revealed the key role of HemN2 in bacterial virulence, which may help us to better understand the strong pathogenicity of the genus Pseudomonas. Compared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying mechanisms haven’t been fully understood. The heme synthesis system is essential for Pseudomonas virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and Pseudomonas virulence were barely pursued. In this study, we hypothesized that hemN2 deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that deletion of hemN2 significantly reduced the virulence of HYS towards C. elegans, whereas the reduction in virulence by the other three genes was not significant. Interestingly, hemN2 deletion significantly reduced colonization of P. donghuensis HYS in the gut of C. elegans. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of P. donghuensis HYS towards C. elegans by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of P. donghuensis HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus Pseudomonas. Simple SummaryPseudomonas donghuensis HYS has lethal virulence towards Caenorhabditis elegans. Anaerobic coproporphyrinogen III oxidase (HemN) is involved in Pseudomonas heme synthesis. However, no research thus far has examined the contribution of HemN to the virulence of Pseudomonas. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that the deletion of the hemN2 gene significantly reduced the virulence of P. donghuensis HYS towards C. elegans. HemN2 was negatively regulated by the Gac system and regulated bacterial virulence via 7-hydroxytropolone (7-HT) synthesis and redox levels. Our findings revealed the key role of HemN2 in bacterial virulence, which may help us to better understand the strong pathogenicity of the genus Pseudomonas.AbstractCompared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying mechanisms haven’t been fully understood. The heme synthesis system is essential for Pseudomonas virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and Pseudomonas virulence were barely pursued. In this study, we hypothesized that hemN2 deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four hemN genes in P. donghuensis HYS, and we reported for the first time that deletion of hemN2 significantly reduced the virulence of HYS towards C. elegans, whereas the reduction in virulence by the other three genes was not significant. Interestingly, hemN2 deletion significantly reduced colonization of P. donghuensis HYS in the gut of C. elegans. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of P. donghuensis HYS towards C. elegans by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of P. donghuensis HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus Pseudomonas. |
| Audience | Academic |
| Author | Lorimer, George H Xiao, Yaqian Gao, Donghao Bayram, Hasan Ghiladi, Reza A Wang, Jun Ma, Xuerui Xie, Zhixiong Xiang, Wang |
| AuthorAffiliation | 6 Department of Chemistry, North Carolina State University, Raleigh, NC 27695, USA; reza_ghiladi@ncsu.edu 2 International Center for Redox Biology & Precision Medicine of Hubei Province, Hubei University of Technology, Wuhan 430068, China 5 Department of Chemistry, University of Maryland, College Park, MD 20742, USA; glorimer@umd.edu 3 Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, China; 2021202040036@whu.edu.cn 4 Department of Pulmonary Medicine, School of Medicine, Koc University, 34010 Istanbul, Turkey; habayram@ku.edu.tr 1 Cooperative Innovation Center of Industrial Fermentation, Ministry of Education & Hubei Province, Hubei University of Technology, Wuhan 430068, China; xiaoyaqian@hbut.edu.cn (Y.X.); xiangwang@hbut.edu.cn (W.X.); 2010511235@hbut.edu.cn (X.M.) |
| AuthorAffiliation_xml | – name: 1 Cooperative Innovation Center of Industrial Fermentation, Ministry of Education & Hubei Province, Hubei University of Technology, Wuhan 430068, China; xiaoyaqian@hbut.edu.cn (Y.X.); xiangwang@hbut.edu.cn (W.X.); 2010511235@hbut.edu.cn (X.M.) – name: 3 Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, China; 2021202040036@whu.edu.cn – name: 6 Department of Chemistry, North Carolina State University, Raleigh, NC 27695, USA; reza_ghiladi@ncsu.edu – name: 2 International Center for Redox Biology & Precision Medicine of Hubei Province, Hubei University of Technology, Wuhan 430068, China – name: 4 Department of Pulmonary Medicine, School of Medicine, Koc University, 34010 Istanbul, Turkey; habayram@ku.edu.tr – name: 5 Department of Chemistry, University of Maryland, College Park, MD 20742, USA; glorimer@umd.edu |
| Author_xml | – sequence: 1 givenname: Yaqian surname: Xiao fullname: Xiao, Yaqian organization: Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, China – sequence: 2 givenname: Wang surname: Xiang fullname: Xiang, Wang organization: International Center for Redox Biology & Precision Medicine of Hubei Province, Hubei University of Technology, Wuhan 430068, China – sequence: 3 givenname: Xuerui surname: Ma fullname: Ma, Xuerui organization: International Center for Redox Biology & Precision Medicine of Hubei Province, Hubei University of Technology, Wuhan 430068, China – sequence: 4 givenname: Donghao surname: Gao fullname: Gao, Donghao organization: Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, China – sequence: 5 givenname: Hasan orcidid: 0000-0002-5236-766X surname: Bayram fullname: Bayram, Hasan organization: Department of Pulmonary Medicine, School of Medicine, Koc University, 34010 Istanbul, Turkey – sequence: 6 givenname: George H surname: Lorimer fullname: Lorimer, George H organization: Department of Chemistry, University of Maryland, College Park, MD 20742, USA – sequence: 7 givenname: Reza A orcidid: 0000-0002-6450-9311 surname: Ghiladi fullname: Ghiladi, Reza A organization: Department of Chemistry, North Carolina State University, Raleigh, NC 27695, USA – sequence: 8 givenname: Zhixiong surname: Xie fullname: Xie, Zhixiong organization: Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan 430072, China – sequence: 9 givenname: Jun surname: Wang fullname: Wang, Jun organization: International Center for Redox Biology & Precision Medicine of Hubei Province, Hubei University of Technology, Wuhan 430068, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38927253$$D View this record in MEDLINE/PubMed |
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| Keywords | HemN2 Pseudomonas donghuensis HYS GacS 7-hydroxytropolone oxidative stress |
| Language | English |
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| Snippet | Compared to pathogens
and
,
HYS has stronger virulence towards
. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is... Compared to pathogens Pseudomonas aeruginosa and P. putida, P. donghuensis HYS has stronger virulence towards Caenorhabditis elegans. However, the underlying... Pseudomonas donghuensis HYS has lethal virulence towards Caenorhabditis elegans. Anaerobic coproporphyrinogen III oxidase (HemN) is involved in Pseudomonas... Simple SummaryPseudomonas donghuensis HYS has lethal virulence towards Caenorhabditis elegans. Anaerobic coproporphyrinogen III oxidase (HemN) is involved in... |
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| SubjectTerms | 7-hydroxytropolone Antibiotics Antifungal agents Antioxidants Bacteria Caenorhabditis elegans E coli Enzymes GacS Gene deletion Genes Genetic engineering Heme HemN2 Immune system Methicillin Methylene blue Nitrates Nitric oxide Oxidative stress Pathogenicity Pathogens Plasmids Pseudomonas Pseudomonas donghuensis HYS Staphylococcus infections Toxicity Virulence Virulence factors Zebrafish |
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| Title | HemN2 Regulates the Virulence of Pseudomonas donghuensis HYS through 7-Hydroxytropolone Synthesis and Oxidative Stress |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/38927253 https://www.proquest.com/docview/3072280800 https://www.proquest.com/docview/3072802164 https://pubmed.ncbi.nlm.nih.gov/PMC11200716 https://doaj.org/article/9a5b04520fe748bba4632e8fd5438e59 |
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