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Effects of Toxin-Antitoxin System HicAB on Biofilm Formation by Extraintestinal Pathogenic E. coli

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Abstract

The type II toxin-antitoxin (T-A) HicAB system is abundant in several bacteria and archaea, such as Escherichia coli, Burkholderia Pseudomallei, Yersinia pestis, Pseudomonas aeruginosa, and Streptococcus pneumoniae. This system engages in stress response, virulence, and bacterial persistence. This study showed that the biofilm-forming ability of the hicAB deletion mutant was significantly decreased to moderate ability compared to the extra-intestinal pathogenic Escherichia coli (ExPEC) parent strain and the complemented strain, which are strong biofilm producers. Congo red assay showed that the hicAB mutant maintained the ability to form curli fimbriae. Using RNA-seq and comparative real-time quantitative RT-PCR, we observed the difference in gene expression between the hicAB mutant and the parent strain, which was associated with biofilm formation. Our data indicate that the HicAB type II T-A system has a key role in biofilm formation by ExPEC, which may be associated with outer membrane protein (OMP) gene expression. Collectively, our results indicate that the hicAB type II T-A system is involved in ExPEC biofilm formation.

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Data Availability

The raw reads were deposited into the NCBI Sequence Read Archive (SRA) database (BioSample Accession Number: SAMN31830681, SAMN31830682; BioProject PRJNA904110).

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Acknowledgements

The authors declare they have no acknowledgements.

Funding

This work was supported by the National Natural Science Foundation of China (Grant Number 31802190 to B Hou) and the Natural Science Foundation of Fujian Province (Grant Number 2018J05053 to B Hou).

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BH and SWL conceived and designed the research. BH did the bioinformatics analyses and wrote the manuscript. CYW, YLC, and QYC helped conducting the experiments. LJZ helped designing the study.

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Correspondence to Bo Hou or Lun-Jiang Zhou.

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Hou, B., Wang, CY., Li, SW. et al. Effects of Toxin-Antitoxin System HicAB on Biofilm Formation by Extraintestinal Pathogenic E. coli. Curr Microbiol 80, 50 (2023). https://doi.org/10.1007/s00284-022-03138-3

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