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Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila

Bacterial antibiotic resistance is a serious global problem; the underlying regulatory mechanisms are largely elusive. The earlier reports states that the vital role of transcriptional regulators (TRs) in bacterial antibiotic resistance. Therefore, we have investigated the role of TRs on enoxacin (E...

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Autores principales: Li, Zhen, Zhang, Lishan, Song, Qingli, Wang, Guibin, Yang, Wenxiao, Tang, Huamei, Srinivasan, Ramanathan, Lin, Ling, Lin, Xiangmin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8217646/
https://www.ncbi.nlm.nih.gov/pubmed/34168639
http://dx.doi.org/10.3389/fmicb.2021.699415
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author Li, Zhen
Zhang, Lishan
Song, Qingli
Wang, Guibin
Yang, Wenxiao
Tang, Huamei
Srinivasan, Ramanathan
Lin, Ling
Lin, Xiangmin
author_facet Li, Zhen
Zhang, Lishan
Song, Qingli
Wang, Guibin
Yang, Wenxiao
Tang, Huamei
Srinivasan, Ramanathan
Lin, Ling
Lin, Xiangmin
author_sort Li, Zhen
collection PubMed
description Bacterial antibiotic resistance is a serious global problem; the underlying regulatory mechanisms are largely elusive. The earlier reports states that the vital role of transcriptional regulators (TRs) in bacterial antibiotic resistance. Therefore, we have investigated the role of TRs on enoxacin (ENX) resistance in Aeromonas hydrophila in this study. A label-free quantitative proteomics method was utilized to compare the protein profiles of the ahslyA knockout and wild-type A. hydrophila strains under ENX stress. Bioinformatics analysis showed that the deletion of ahslyA triggers the up-regulated expression of some vital antibiotic resistance proteins in A. hydrophila upon ENX stress and thereby reduce the pressure by preventing the activation of SOS repair system. Moreover, ahslyA directly or indirectly induced at least 11 TRs, which indicates a complicated regulatory network under ENX stress. We also deleted six selected genes in A. hydrophila that altered in proteomics data in order to evaluate their roles in ENX stress. Our results showed that genes such as AHA_0655, narQ, AHA_3721, AHA_2114, and AHA_1239 are regulated by ahslyA and may be involved in ENX resistance. Overall, our data demonstrated the important role of ahslyA in ENX resistance and provided novel insights into the effects of transcriptional regulation on antibiotic resistance in bacteria.
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spelling pubmed-82176462021-06-23 Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila Li, Zhen Zhang, Lishan Song, Qingli Wang, Guibin Yang, Wenxiao Tang, Huamei Srinivasan, Ramanathan Lin, Ling Lin, Xiangmin Front Microbiol Microbiology Bacterial antibiotic resistance is a serious global problem; the underlying regulatory mechanisms are largely elusive. The earlier reports states that the vital role of transcriptional regulators (TRs) in bacterial antibiotic resistance. Therefore, we have investigated the role of TRs on enoxacin (ENX) resistance in Aeromonas hydrophila in this study. A label-free quantitative proteomics method was utilized to compare the protein profiles of the ahslyA knockout and wild-type A. hydrophila strains under ENX stress. Bioinformatics analysis showed that the deletion of ahslyA triggers the up-regulated expression of some vital antibiotic resistance proteins in A. hydrophila upon ENX stress and thereby reduce the pressure by preventing the activation of SOS repair system. Moreover, ahslyA directly or indirectly induced at least 11 TRs, which indicates a complicated regulatory network under ENX stress. We also deleted six selected genes in A. hydrophila that altered in proteomics data in order to evaluate their roles in ENX stress. Our results showed that genes such as AHA_0655, narQ, AHA_3721, AHA_2114, and AHA_1239 are regulated by ahslyA and may be involved in ENX resistance. Overall, our data demonstrated the important role of ahslyA in ENX resistance and provided novel insights into the effects of transcriptional regulation on antibiotic resistance in bacteria. Frontiers Media S.A. 2021-06-08 /pmc/articles/PMC8217646/ /pubmed/34168639 http://dx.doi.org/10.3389/fmicb.2021.699415 Text en Copyright © 2021 Li, Zhang, Song, Wang, Yang, Tang, Srinivasan, Lin and Lin. 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 Microbiology
Li, Zhen
Zhang, Lishan
Song, Qingli
Wang, Guibin
Yang, Wenxiao
Tang, Huamei
Srinivasan, Ramanathan
Lin, Ling
Lin, Xiangmin
Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title_full Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title_fullStr Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title_full_unstemmed Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title_short Proteomics Analysis Reveals Bacterial Antibiotics Resistance Mechanism Mediated by ahslyA Against Enoxacin in Aeromonas hydrophila
title_sort proteomics analysis reveals bacterial antibiotics resistance mechanism mediated by ahslya against enoxacin in aeromonas hydrophila
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8217646/
https://www.ncbi.nlm.nih.gov/pubmed/34168639
http://dx.doi.org/10.3389/fmicb.2021.699415
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