The Molecular Mechanisms Regulating Stress-Adaptive Responses in Bacteria

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Antimicrobial Agents and Resistance".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 421

Special Issue Editors


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Guest Editor
Department of General and Medical Biochemistry, Faculty of Biology, University of Gdansk, Wita Stwosza 59, 80-308 Gdańsk, Poland
Interests: bacterial physiology; biofilm; bacterial stress responses; heat shock proteins; antibiotic tolerance

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Guest Editor Assistant
Department of Medicine, Division of Gastroenterology and Hepatology, Pennsylvania State University College of Medicine, Hershey, PA, USA
Interests: biofilms; strategies to combat antimicrobial resistance; inflammatory bowel disease and tight junction

Special Issue Information

Dear Colleagues,

Bacteria combat an array of stresses in their natural setting, which elicit a variety of adaptive responses as a survival mechanism. Effective adaptive response ensues in bacterial persistence, antibiotic resistance, biofilm formation and resistance development. Understanding the intricacy of mechanisms governing the adaptation can support the advancement of suitable antimicrobials. This Special Issue brings together the cutting-edge research studies exploring the molecular mechanisms in bacterial stress adaptation, emphasizing signal transduction pathways, transcriptional and translational regulations, metabolic reprogramming, etc.

Key topics include two component regulatory systems, toxin–antitoxin systems and small regulatory RNAs in coordinating stress response. We also feature insights on bacterial persistence strategies, such as biofilm formation and virulence development and their implications on antibiotic resistance and pathogenesis. By elucidating these mechanisms, this collection aims to expand our knowledge about bacterial resilience and inform novel antimicrobial strategies.

We invite researchers to contribute to this Special Issue, which offers to impart recent discoveries in bacterial stress adaptation and promote new avenues in infectious disease research.

Dr. Ewa Laskowska
Guest Editor

Dr. Arumugam Priya
Guest Editor Assistant

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Keywords

  • biofilms
  • strategies to combat antimicrobial resistance
  • bacterial stress adaptation

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Published Papers (1 paper)

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Research

15 pages, 4058 KB  
Article
SpuA-Mediated Glycogen Metabolism Modulates Acid Stress Adaptation via Formic Acid and Amino Acid Utilization in Streptococcus pneumoniae
by Weichen Gong, Masayuki Ono, Xuefei Cheng, Yujiro Hirose, Keita Nishiyama, Haruki Kitazawa and Shigetada Kawabata
Microorganisms 2025, 13(10), 2409; https://doi.org/10.3390/microorganisms13102409 - 21 Oct 2025
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Abstract
Glycogen metabolism plays a key role in bacterial adaptation. In Streptococcus pneumoniae, the glycogen-degrading enzyme SpuA is widely conserved, but its physiological significance remains unclear. In this study, we investigated how SpuA affects bacterial growth and response to acid stress. We found [...] Read more.
Glycogen metabolism plays a key role in bacterial adaptation. In Streptococcus pneumoniae, the glycogen-degrading enzyme SpuA is widely conserved, but its physiological significance remains unclear. In this study, we investigated how SpuA affects bacterial growth and response to acid stress. We found that the spuA deletion strain (ΔspuA) produced more acidic metabolites under anaerobic conditions than the wild-type strain. In a mouse infection model, bronchoalveolar lavage fluid (BALF) from ΔspuA-infected mice was more acidic on day 1 post-infection, showing a lower bacterial load than wild-type infection—a finding consistent with the early growth delay observed in vitro—but the mutant later exhibited enhanced persistence at 72 h. ΔspuA strains also showed greater tolerance to formic acid and higher intake of serum amyloid A1 (SAA1), which may further contribute to their survival in acidic environments. Transcriptomic analysis revealed reduced utilization of certain amino acids, particularly cysteine, in ΔspuA strains. However, the addition of 0.05% (v/v) formic acid restored amino acid utilization in ΔspuA strains, and co-supplementation with formic acid and cysteine significantly enhanced ΔspuA growth in vitro. These findings suggest that in the absence of SpuA, S. pneumoniae shifts its metabolism toward formic acid production, which may act both as a metabolic signal and a stressor that influences bacterial gene expression. This shift is accompanied by increased expression of tRNAs and growth rescue, suggesting enhanced amino acid utilization capacity. Although our findings reveal a potential link between formic acid metabolism and amino acid utilization through tRNA regulation, further validation using metabolic flux analyses or targeted metabolomics will be required to confirm this relationship. These observations imply a metabolic adaptation that facilitates bacterial growth under low-oxygen, acidic conditions during infection. Our results also raise the possibility that SpuA plays a role in restraining bacterial overgrowth in the host, thereby promoting a more balanced coexistence between pathogen and host. Full article
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