{
  "abstract": "During infection, Klebsiella pneumoniae must withstand host-derived oxidative stress not only by detoxifying reactive oxygen species (ROS) but also by repairing oxidative damage to cellular physiology. How these detoxification and stress-adaptive responses are coordinated remains unclear. Here, we identify a plasmid-encoded tacAT locus as an OxyR-responsive regulatory module that supports peroxide tolerance and in vivo fitness in K. pneumoniae. Guided by the conservation of the OxyR DNA-binding domain and its consensus binding motif, we surveyed promoter-proximal regions of the K. pneumoniae CRK3022 chromosome and plasmids for candidate OxyR-responsive loci. This analysis identified tacAT, a putative type II toxin-antitoxin (TA) module, as the only plasmid-associated candidate. OxyR directly bound the tacAT promoter and contributed to tacAT induction during hydrogen peroxide (H?O?) stress. The TacAT complex exhibited DNA-binding and transcriptional regulatory activity, promoting the expression of genes linked to protein quality control and membrane/envelope homeostasis, including clpB, htpG, cadC, bhsA, and marA. Deletion of tacAT compromised survival under lethal peroxide challenge and attenuated bacterial dissemination, tissue pathology, and inflammatory responses in a murine bacteremia model. These findings define an OxyR-TacAT regulatory branch that connects peroxide sensing with stress-adaptive gene expression, revealing how a TA-associated module can be integrated into stress-adaptive programs during host-associated oxidative stress.",
  "abstract_shown": true,
  "affiliations": [
    "West China Hospital of Sichuan University"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 12,
  "authors": [
    {
      "name": "J. Zhou"
    },
    {
      "name": "H. Ma"
    },
    {
      "name": "Z. Sha"
    },
    {
      "name": "S. Liu"
    },
    {
      "name": "J. Rao"
    },
    {
      "name": "N. Zhao"
    },
    {
      "name": "X. Mou"
    },
    {
      "name": "C. Chen"
    },
    {
      "name": "H. Li"
    },
    {
      "name": "H. Liu"
    },
    {
      "name": "H. Wu"
    },
    {
      "affs": [
        0
      ],
      "name": "R. Bao"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/9x7hhzz174k2c.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.23.753711",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.23.753711v1.full",
  "id": "9x7hhzz174k2c",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.23.753711v1",
  "language": null,
  "licence": "CC-BY-NC-ND",
  "licence_label": "CC BY-NC-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "microbiology"
    ],
    [
      "openalex",
      "1311|Bacterial Genetics and Biotechnology"
    ]
  ],
  "openalex": "W7214190926",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.23.753711v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-23",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/9x7hhzz174k2c.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:24:25Z",
      "native_id": "10.64898/2026.09.23.753711",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.23.753711v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:microbiology",
      "subfield": "microbiology"
    }
  ],
  "title": "The OxyR-Responsive TacAT Module Promotes Oxidative Stress Adaptation and In Vivo Fitness in K. pneumoniae",
  "title_text": "The OxyR-Responsive TacAT Module Promotes Oxidative Stress Adaptation and In Vivo Fitness in K. pneumoniae",
  "type": "preprint",
  "updated_at": "2026-10-30T12:24:25Z",
  "url": "https://research.draconitic.com/paper/9x7hhzz174k2c",
  "venue": "bioRxiv",
  "versions": []
}