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LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
Acinetobacter baumannii is an important nosocomial pathogen that can survive in different environmental conditions and poses a severe threat to public health due to its multidrug resistance properties. Research on transcriptional regulators, which play an essential role in adjusting to new environme...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8543017/ https://www.ncbi.nlm.nih.gov/pubmed/34708004 http://dx.doi.org/10.3389/fcimb.2021.738706 |
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author | Islam, Md. Maidul Kim, Kyeongmin Lee, Je Chul Shin, Minsang |
author_facet | Islam, Md. Maidul Kim, Kyeongmin Lee, Je Chul Shin, Minsang |
author_sort | Islam, Md. Maidul |
collection | PubMed |
description | Acinetobacter baumannii is an important nosocomial pathogen that can survive in different environmental conditions and poses a severe threat to public health due to its multidrug resistance properties. Research on transcriptional regulators, which play an essential role in adjusting to new environments, could provide new insights into A. baumannii pathogenesis. LysR-type transcriptional regulators (LTTRs) are structurally conserved among bacterial species and regulate virulence in many pathogens. We identified a novel LTTR, designated as LeuO encoded in the A. baumannii genome. After construction of LeuO mutant strain, transcriptome analysis showed that LeuO regulates the expression of 194 upregulated genes and 108 downregulated genes responsible for various functions and our qPCR validation of several differentially expressed genes support transcriptome data. Our results demonstrated that disruption of LeuO led to increased biofilm formation and increased pathogenicity in an animal model. However, the adherence and surface motility of the LeuO mutant were reduced compared with those of the wild-type strain. We observed some mutations on amino acids sequence of LeuO in clinical isolates. These mutations in the A. baumannii biofilm regulator LeuO may cause hyper-biofilm in the tested clinical isolates. This study is the first to demonstrate the association between the LTTR member LeuO and virulence traits of A. baumannii. |
format | Online Article Text |
id | pubmed-8543017 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85430172021-10-26 LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii Islam, Md. Maidul Kim, Kyeongmin Lee, Je Chul Shin, Minsang Front Cell Infect Microbiol Cellular and Infection Microbiology Acinetobacter baumannii is an important nosocomial pathogen that can survive in different environmental conditions and poses a severe threat to public health due to its multidrug resistance properties. Research on transcriptional regulators, which play an essential role in adjusting to new environments, could provide new insights into A. baumannii pathogenesis. LysR-type transcriptional regulators (LTTRs) are structurally conserved among bacterial species and regulate virulence in many pathogens. We identified a novel LTTR, designated as LeuO encoded in the A. baumannii genome. After construction of LeuO mutant strain, transcriptome analysis showed that LeuO regulates the expression of 194 upregulated genes and 108 downregulated genes responsible for various functions and our qPCR validation of several differentially expressed genes support transcriptome data. Our results demonstrated that disruption of LeuO led to increased biofilm formation and increased pathogenicity in an animal model. However, the adherence and surface motility of the LeuO mutant were reduced compared with those of the wild-type strain. We observed some mutations on amino acids sequence of LeuO in clinical isolates. These mutations in the A. baumannii biofilm regulator LeuO may cause hyper-biofilm in the tested clinical isolates. This study is the first to demonstrate the association between the LTTR member LeuO and virulence traits of A. baumannii. Frontiers Media S.A. 2021-10-11 /pmc/articles/PMC8543017/ /pubmed/34708004 http://dx.doi.org/10.3389/fcimb.2021.738706 Text en Copyright © 2021 Islam, Kim, Lee and Shin https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cellular and Infection Microbiology Islam, Md. Maidul Kim, Kyeongmin Lee, Je Chul Shin, Minsang LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii |
title | LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
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title_full | LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
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title_fullStr | LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
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title_full_unstemmed | LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
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title_short | LeuO, a LysR-Type Transcriptional Regulator, Is Involved in Biofilm Formation and Virulence of Acinetobacter baumannii
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title_sort | leuo, a lysr-type transcriptional regulator, is involved in biofilm formation and virulence of acinetobacter baumannii |
topic | Cellular and Infection Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8543017/ https://www.ncbi.nlm.nih.gov/pubmed/34708004 http://dx.doi.org/10.3389/fcimb.2021.738706 |
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