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AbaR is a LuxR type regulator essential for motility and the formation of biofilm and pellicle in Acinetobacter baumannii

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Abstract

Background

Acinetobacter baumannii is a major opportunistic pathogen causing nosocomial infections. Acinetobacter baumannii possesses a quorum sensing system consisting of abaI, encoding an autoinducer synthase, and abaR, encoding a putative LuxR type regulator. AbaI is required for motility and biofilm formation in A. baumannii. However, the functions of AbaR on the expression of abaI, motility, and the formation of biofilm and pellicle have not yet been explored.

Objective

The aim of this study was to investigate the effects of abaR mutation on the expression of abaI, motility, and the formation of biofilm and pellicle.

Methods

Functions of AbaR were assessed by the construction of an isogenic mutant and by evaluating the effects of abaR mutation on the expression of abaI, motility, and the formation of biofilm and pellicle.

Results

The abaR mutant revealed a significant decrease in the expression of abaI. The disruption of abaR resulted in substantial defects in motility and the formation of biofilm and pellicle. Introduction of abaR in trans complemented the defects.

Conclusions

AbaR of A. baumannii is required for the expression of abaI and plays important roles in motility and the formation of biofilm and pellicle. AbaR may be considered to be a target of anti-biofilm agents.

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Acknowledgements

The authors gratefully acknowledge the Center for Bio-Medical Engineering Core Facility at Dankook University for providing critical reagents and equipment.

Funding

This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health and Welfare, Republic of Korea (Grant number HI17C1657).

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Correspondence to Kyudong Han.

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Oh, M.H., Han, K. AbaR is a LuxR type regulator essential for motility and the formation of biofilm and pellicle in Acinetobacter baumannii. Genes Genom 42, 1339–1346 (2020). https://doi.org/10.1007/s13258-020-01005-8

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