qsmR encoding an IclR-family transcriptional factor is a core pathogenic determinant of Burkholderia glumae beyond the acyl-homoserine lactone-mediated quorum-sensing system.

Autor: Lelis TP; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America., Bruno J; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America., Padilla J; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America., Barphagha I; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America., Ontoy J; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America., Ham JH; Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, Louisiana, United States of America.
Jazyk: angličtina
Zdroj: PLoS pathogens [PLoS Pathog] 2024 Oct 03; Vol. 20 (10), pp. e1011862. Date of Electronic Publication: 2024 Oct 03 (Print Publication: 2024).
DOI: 10.1371/journal.ppat.1011862
Abstrakt: The plant pathogenic bacterium Burkholderia glumae causes bacterial panicle blight (BPB) in rice-growing areas worldwide. It has been widely accepted that an acyl-homoserine lactone (AHL)-type quorum sensing (QS) system encoded by tofI and tofR genes (TofIR QS) is a key regulatory mechanism underlying the bacterial pathogenesis of B. glumae. In addition, qsmR, which encodes an IclR-family regulatory protein, has been considered an important part of TofIR QS. However, the present study with three strains of B. glumae representing different pathogenic strains revealed that this currently accepted paradigm should be modified. We characterized the regulatory function of TofIR QS and qsmR in three different strains of B. glumae, 336gr-1 (virulent), 411gr-6 (hypervirulent) and 257sh-1 (avirulent). In 336gr-1, both TofIR QS and qsmR were critical for the pathogenesis, being consistent with previous studies. However, in the hypervirulent strain 411gr-6, TofIR QS only partially contributes to the virulence, whereas qsmR was critical for pathogenesis like in 336gr-1. Furthermore, we found that a single nucleotide polymorphism causing T50K substitution in the qsmR coding sequence was the cause of the non-pathogenic trait of the naturally avirulent strain 257sh-1. Subsequent analyses of gene expression and transcriptome revealed that TofIR QS is partially controlled by qsmR at the transcriptional level in both virulent strains. Further genetic tests of additional B. glumae strains showed that 11 out of 20 virulent strains retained the ability to produce toxoflavin even after removing the tofI/tofM/tofR QS gene cluster like 411gr-6. In contrast, all the virulent strains tested lost the ability to produce toxoflavin almost completely upon deletion of the qsmR gene. Taking these results together, qsmR, rather than TofIR QS, is a master regulator that determines the pathogenic trait of B. glumae thus a more appropriate pathogen target for successful management of BPB.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Lelis et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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