ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Antimicrobials, Resistance and Chemotherapy
This article is part of the Research TopicMicrobial Metabolites to Combat Antimicrobial ResistanceView all articles
Regulatory Relationships Among aldB, ampH, and acoR and Their Impact on β-Lactam Susceptibility in Phytobacter diazotrophicus
Provisionally accepted
- Quanzhou Women's and Children's Hospital, Quanzhou, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: Phytobacter diazotrophicus (P. diazotrophicus) is an emerging opportunistic pathogen responsible for various human infections. This study aims to explore the association between the aldB gene and bacterial susceptibility to β-lactam antibiotics, investigate the potential mechanism by which aldB mediates antibiotic resistance, and clarify the regulatory mechanism of aldB by the upstream adjacent gene acoR. Methods: The MICs of 12 β-lactam antibiotics were determined using the MH agar plate dilution method. RNA transcriptome analysis was performed on the wild-type and aldB knockout strains of P. diazotrophicus Pd1. mRNA expression levels were measured using qPCR .The binding of the purified AcoR-HTH protein to PaldB was analyzed using EMSA. Ceftazidime was used for antibiotic stimulation tests. Results: Compared with the wild-type strain, the aldB knockout strain exhibited significantly increased MICs for carbenicillin, cefalotin, cefoxitin, cefuroxime, cefotaxime, ceftazidime, cefepime, and aztreonam . RNA transcriptome sequencing revealed that ampH was most significantly downregulated in the aldB knockout strain, which was confirmed by qPCR. Compared with the wild-type strain, the ampH-knockout strain exhibited significantly increased MICs for carbenicillin, piperacillin, cefalotin, cefoxitin, cefuroxime, cefotaxime, ceftazidime, cefepime, aztreonam, and ertapenem. Compared with the wild-type strain, the acoR knockout strain exhibited significantly increased MICs for carbenicillin, piperacillin, cefalotin, cefoxitin, cefuroxime, cefotaxime, ceftazidime, cefepime, aztreonam, and ertapenem by at least 2-, 4-, 4-, 8-, 4-, 8-, 8-, 4-, 4-, and 2-fold, respectively. Compared with the wild-type strain, the acoR knockout strain significantly downregulates the mRNA expression of aldB. The sequence ACGACACAGTTCGCGAA was identified as a recognition site for AcoR in P. diazotrophicus through software alignment and EMSA experiments. Compared with the untreated wild-type strain, aldB mRNA expression levels in the ceftazidime-stimulated wild-type strain reduced significantly. Conclusion: In P. diazotrophicus, aldB and acoR reduced some β-lactam resistance by facilitating ampH and aldB expression, respectively. This is the first report that links acoR to β-lactam antibiotics and demonstrates that AcoR positively regulates aldB. Under ceftazidime stress, P. diazotrophicus reduced aldB expression to increase its tolerance to the antibiotic.The discovery of the mechanism by which AcoR regulates aldB expression provides preliminary evidence for subsequent research on drug resistance mechanisms.
Keywords: P. diazotrophicus, aldB, AMPH, ACOR, antibiotic resistance
Received: 17 Aug 2025; Accepted: 27 Oct 2025.
Copyright: © 2025 Lin, Zheng and Wang. 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) or licensor 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.
* Correspondence: Jiansheng Lin, 63678462@qq.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.