Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426
Abstract Background The inner membrane protein DotU of Aeromonas veronii is an important component of the minimal core conserved membrane proteome required for the formation of an envelope-transmembrane complex. This protein functions in a type VI secretion system (T6SS), and the role of this T6SS d...
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BMC
2020-04-01
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Series: | BMC Microbiology |
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Online Access: | http://link.springer.com/article/10.1186/s12866-020-01743-5 |
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author | Haichao Song Yuanhuan Kang Aidong Qian Xiaofeng Shan Ying Li Lei Zhang Haipeng Zhang Wuwen Sun |
author_facet | Haichao Song Yuanhuan Kang Aidong Qian Xiaofeng Shan Ying Li Lei Zhang Haipeng Zhang Wuwen Sun |
author_sort | Haichao Song |
collection | DOAJ |
description | Abstract Background The inner membrane protein DotU of Aeromonas veronii is an important component of the minimal core conserved membrane proteome required for the formation of an envelope-transmembrane complex. This protein functions in a type VI secretion system (T6SS), and the role of this T6SS during the pathogenic process has not been clearly described. Results A recombinant A. veronii with a partial disruption of the dotU gene (720 bp of the in-frame sequence) (defined as ∆dotU) was constructed by two conjugate exchanges. We found that the mutant ∆dotU allele can be stably inherited for more than 50 generations. Inactivation of the A. veronii dotU gene resulted in no significant changes in growth or resistance to various environmental changes. However, compared with the wild-type strain colony, the mutant ∆dotU colony had a rough surface morphology. In addition, the biofilm formation ability of the mutant ∆dotU was significantly enhanced by 2.1-fold. Conversely, the deletion of the dotU gene resulted in a significant decrease in pathogenicity and infectivity compared to those of the A. veronii wild-type strain. Conclusions Our findings indicated that the dotU gene was an essential participant in the pathogenicity and invasiveness of A. veronii TH0426, which provides a novel perspective on the pathogenesis of TH0426 and lays the foundation for discovering potential T6SS effectors. |
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language | English |
last_indexed | 2024-12-20T17:40:09Z |
publishDate | 2020-04-01 |
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spelling | doaj.art-ecfbb9bd7d9e4cf0b93b5d63b77115c82022-12-21T19:31:08ZengBMCBMC Microbiology1471-21802020-04-0120111110.1186/s12866-020-01743-5Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426Haichao Song0Yuanhuan Kang1Aidong Qian2Xiaofeng Shan3Ying Li4Lei Zhang5Haipeng Zhang6Wuwen Sun7College of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityCollege of Animal Science and Technology, Jilin Agricultural UniversityAbstract Background The inner membrane protein DotU of Aeromonas veronii is an important component of the minimal core conserved membrane proteome required for the formation of an envelope-transmembrane complex. This protein functions in a type VI secretion system (T6SS), and the role of this T6SS during the pathogenic process has not been clearly described. Results A recombinant A. veronii with a partial disruption of the dotU gene (720 bp of the in-frame sequence) (defined as ∆dotU) was constructed by two conjugate exchanges. We found that the mutant ∆dotU allele can be stably inherited for more than 50 generations. Inactivation of the A. veronii dotU gene resulted in no significant changes in growth or resistance to various environmental changes. However, compared with the wild-type strain colony, the mutant ∆dotU colony had a rough surface morphology. In addition, the biofilm formation ability of the mutant ∆dotU was significantly enhanced by 2.1-fold. Conversely, the deletion of the dotU gene resulted in a significant decrease in pathogenicity and infectivity compared to those of the A. veronii wild-type strain. Conclusions Our findings indicated that the dotU gene was an essential participant in the pathogenicity and invasiveness of A. veronii TH0426, which provides a novel perspective on the pathogenesis of TH0426 and lays the foundation for discovering potential T6SS effectors.http://link.springer.com/article/10.1186/s12866-020-01743-5Aeromonas veroniiVirulenceT6SSPathogenicitydotU |
spellingShingle | Haichao Song Yuanhuan Kang Aidong Qian Xiaofeng Shan Ying Li Lei Zhang Haipeng Zhang Wuwen Sun Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 BMC Microbiology Aeromonas veronii Virulence T6SS Pathogenicity dotU |
title | Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 |
title_full | Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 |
title_fullStr | Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 |
title_full_unstemmed | Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 |
title_short | Inactivation of the T6SS inner membrane protein DotU results in severe attenuation and decreased pathogenicity of Aeromonas veronii TH0426 |
title_sort | inactivation of the t6ss inner membrane protein dotu results in severe attenuation and decreased pathogenicity of aeromonas veronii th0426 |
topic | Aeromonas veronii Virulence T6SS Pathogenicity dotU |
url | http://link.springer.com/article/10.1186/s12866-020-01743-5 |
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