The bacteriophage transcription factor Gp53 suppresses cell division and regulates Pseudomonas aeruginosa physiology
Abstract
Pseudomonas aeruginosa is a highly drug-resistant pathogen that poses a major challenge to clinical treatment. Bacteriophages encode diverse regulatory proteins that can alter host cellular processes during infection. Here we show that the ΦPA1019-encoded transcription factor Gp53 regulates bacterial physiology by targeting key host pathways. Gp53 expression reduces bacterial growth, motility, and biofilm formation, and causes filamentous cell morphology. Transcriptomic analysis reveals that Gp53 alters the expression of 3,342 genes, including genes involved in cell division and virulence-associated processes. DNA-binding assays demonstrate that Gp53 directly represses promoters of key host genes, including ftsZ , fleQ , pslA , and amrZ . Gp53-mediated repression of ftsZ disrupts Z-ring formation and inhibits cell division, while ftsZ expression restores these defects. Structural and mutational analyses identify residues important for Gp53-DNA interaction. Together, these findings reveal a phage-encoded mechanism that coordinately interferes with bacterial cell division and virulence-associated pathways, providing mechanistic insights into host transcriptional regulation during phage infection and expanding our understanding of phage-host interactions.
Related
- Refractory Pseudomonas aeruginosa Bronchopulmonary Infection After Lung Transplantation for Common Variable Immunodeficiency Despite Maximal Treatment Including IgM/IgA-Enriched Immunoglobulins and Bacteriophage Therapy
- Bacteriophage PAK_P3 genome structuration and dynamics during infection of Pseudomonas aeruginosa reveal specific interaction patterns
- A dual-action bacteriophage protein Ped1 degrades DNA and blocks replication in Pseudomonas aeruginosa
- Bacteriophage and Antibiotic Resistance Are Positively Associated across a Phylogenetically Diverse Set of Clinical Pseudomonas aeruginosa Isolates
- Bacteriophage Therapy in Cystic Fibrosis: Emerging Strategies for Managing Chronic Pseudomonas aeruginosa Infections.
BibTeX
@article{li2026bacteriophage,
title = {{The bacteriophage transcription factor Gp53 suppresses cell division and regulates Pseudomonas aeruginosa physiology}},
author = {Ying Li and Xiaomin Li and Gukui Chen and Lixin Yuan and Hailong Zhong and Min Hui and Yongfeng Sun and Yufei Han and Shuqin Zhou and Shiwei Wang and Weina Kong},
journal = {Communications Biology},
year = {2026},
month = oct,
doi = {10.1038/s42003-026-11031-z},
url = {https://www.nature.com/articles/s42003-026-11031-z},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The bacteriophage transcription factor Gp53 suppresses cell division and regulates Pseudomonas aeruginosa physiology
AU - Ying Li
AU - Xiaomin Li
AU - Gukui Chen
AU - Lixin Yuan
AU - Hailong Zhong
AU - Min Hui
AU - Yongfeng Sun
AU - Yufei Han
AU - Shuqin Zhou
AU - Shiwei Wang
AU - Weina Kong
PY - 2026
DA - 2026/10/08
JO - Communications Biology
DO - 10.1038/s42003-026-11031-z
UR - https://www.nature.com/articles/s42003-026-11031-z
AB - Pseudomonas aeruginosa is a highly drug-resistant pathogen that poses a major challenge to clinical treatment. Bacteriophages encode diverse regulatory proteins that can alter host cellular processes during infection. Here we show that the ΦPA1019-encoded transcription factor Gp53 regulates bacterial physiology by targeting key host pathways. Gp53 expression reduces bacterial growth, motility, and biofilm formation, and causes filamentous cell morphology. Transcriptomic analysis reveals that Gp53 alters the expression of 3,342 genes, including genes involved in cell division and virulence-associated processes. DNA-binding assays demonstrate that Gp53 directly represses promoters of key host genes, including ftsZ , fleQ , pslA , and amrZ . Gp53-mediated repression of ftsZ disrupts Z-ring formation and inhibits cell division, while ftsZ expression restores these defects. Structural and mutational analyses identify residues important for Gp53-DNA interaction. Together, these findings reveal a phage-encoded mechanism that coordinately interferes with bacterial cell division and virulence-associated pathways, providing mechanistic insights into host transcriptional regulation during phage infection and expanding our understanding of phage-host interactions.
SN - 2399-3642
ER -