Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression
Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism...
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| Autor*in: |
Jiang, Ming [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) 2022 |
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| Übergeordnetes Werk: |
Enthalten in: Genes & Genomics - The Genetics Society of Korea, 2010, 45(2022), 2 vom: 15. Dez., Seite 191-202 |
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| Übergeordnetes Werk: |
volume:45 ; year:2022 ; number:2 ; day:15 ; month:12 ; pages:191-202 |
| Links: |
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| DOI / URN: |
10.1007/s13258-022-01352-8 |
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SPR049117203 |
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| 520 | |a Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. | ||
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| 700 | 1 | |a Pan, Ting |4 aut | |
| 700 | 1 | |a Li, Yujie |4 aut | |
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10.1007/s13258-022-01352-8 doi (DE-627)SPR049117203 (SPR)s13258-022-01352-8-e DE-627 ger DE-627 rakwb eng Jiang, Ming verfasserin aut Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. RinA (dpeaa)DE-He213 SarA (dpeaa)DE-He213 Virulence (dpeaa)DE-He213 Li, Yilin aut Sun, Baolin aut Xu, Shiwen aut Pan, Ting aut Li, Yujie aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2022), 2 vom: 15. Dez., Seite 191-202 (DE-627)SPR031096425 nnns volume:45 year:2022 number:2 day:15 month:12 pages:191-202 https://dx.doi.org/10.1007/s13258-022-01352-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 45 2022 2 15 12 191-202 |
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10.1007/s13258-022-01352-8 doi (DE-627)SPR049117203 (SPR)s13258-022-01352-8-e DE-627 ger DE-627 rakwb eng Jiang, Ming verfasserin aut Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. RinA (dpeaa)DE-He213 SarA (dpeaa)DE-He213 Virulence (dpeaa)DE-He213 Li, Yilin aut Sun, Baolin aut Xu, Shiwen aut Pan, Ting aut Li, Yujie aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2022), 2 vom: 15. Dez., Seite 191-202 (DE-627)SPR031096425 nnns volume:45 year:2022 number:2 day:15 month:12 pages:191-202 https://dx.doi.org/10.1007/s13258-022-01352-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 45 2022 2 15 12 191-202 |
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10.1007/s13258-022-01352-8 doi (DE-627)SPR049117203 (SPR)s13258-022-01352-8-e DE-627 ger DE-627 rakwb eng Jiang, Ming verfasserin aut Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. RinA (dpeaa)DE-He213 SarA (dpeaa)DE-He213 Virulence (dpeaa)DE-He213 Li, Yilin aut Sun, Baolin aut Xu, Shiwen aut Pan, Ting aut Li, Yujie aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2022), 2 vom: 15. Dez., Seite 191-202 (DE-627)SPR031096425 nnns volume:45 year:2022 number:2 day:15 month:12 pages:191-202 https://dx.doi.org/10.1007/s13258-022-01352-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 45 2022 2 15 12 191-202 |
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10.1007/s13258-022-01352-8 doi (DE-627)SPR049117203 (SPR)s13258-022-01352-8-e DE-627 ger DE-627 rakwb eng Jiang, Ming verfasserin aut Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. RinA (dpeaa)DE-He213 SarA (dpeaa)DE-He213 Virulence (dpeaa)DE-He213 Li, Yilin aut Sun, Baolin aut Xu, Shiwen aut Pan, Ting aut Li, Yujie aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2022), 2 vom: 15. Dez., Seite 191-202 (DE-627)SPR031096425 nnns volume:45 year:2022 number:2 day:15 month:12 pages:191-202 https://dx.doi.org/10.1007/s13258-022-01352-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 45 2022 2 15 12 191-202 |
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10.1007/s13258-022-01352-8 doi (DE-627)SPR049117203 (SPR)s13258-022-01352-8-e DE-627 ger DE-627 rakwb eng Jiang, Ming verfasserin aut Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. RinA (dpeaa)DE-He213 SarA (dpeaa)DE-He213 Virulence (dpeaa)DE-He213 Li, Yilin aut Sun, Baolin aut Xu, Shiwen aut Pan, Ting aut Li, Yujie aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2022), 2 vom: 15. Dez., Seite 191-202 (DE-627)SPR031096425 nnns volume:45 year:2022 number:2 day:15 month:12 pages:191-202 https://dx.doi.org/10.1007/s13258-022-01352-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 45 2022 2 15 12 191-202 |
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RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. 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phage transcription activator rina regulates staphylococcus aureus virulence by governing sara expression |
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Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression |
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Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. © The Author(s) 2022 |
| abstractGer |
Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. © The Author(s) 2022 |
| abstract_unstemmed |
Background Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Conclusion Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression. © The Author(s) 2022 |
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Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression |
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https://dx.doi.org/10.1007/s13258-022-01352-8 |
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Li, Yilin Sun, Baolin Xu, Shiwen Pan, Ting Li, Yujie |
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Li, Yilin Sun, Baolin Xu, Shiwen Pan, Ting Li, Yujie |
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2024-07-03T23:23:17.915Z |
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RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. Objective We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. Methods The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. Results In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. 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