Crystallization of the N-terminal regulatory domain of the enhancer-binding protein FleQ from<i>Stenotrophomonas maltophilia</i>

Yang, Jauo-Guey; Shih, Ming‐Hsiang; Kuo, Wei‐Ting; Chin, Ko‐Hsin; Chou, Shan‐Ho

doi:10.1107/s2053230x14001514

Cited by 7 publications

(5 citation statements)

References 27 publications

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“…In addition, the genes encoding three transcription regulators ( fleQ , fsnR , and bfmA ) also control biofilm development. FleQ binds to the putative ATPase FleN to form a complex that directs flagellar gene expression 30 . FsnR, designated as a response regulator with transcription-regulating activity, binds directly to the promoter regions of gene clusters involved in flagellar assembly to activate their transcriptional initiation 31 , 32 .…”

Section: Introductionmentioning

confidence: 99%

BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia

Liu

Tian

Wei

et al. 2017

Sci Rep

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c-di-GMP is a cellular second messenger that regulates diverse bacterial processes, including swimming, biofilm formation and virulence. However, in Stenotrophomonas maltophilia, a nosocomial pathogen that frequently infects immunodeficient or immunoincompetent patients, the regulatory function of c-di-GMP remains unclear. Here we show that BsmR is a negative regulator of biofilm development that degrades c-di-GMP through its EAL domain. Increasing BsmR expression resulted in significant increase in bacterial swimming and decrease in cell aggregation. BsmR regulates the expression of at least 349 genes. Among them, 34 involved in flagellar assembly and a flagellar-assembly-related transcription factor (fsnR) are positively regulated. Although BsmR is a response regulator of the two-component signaling system, its role in biofilm formation depends on the expression level of its respective gene (bsmR), not on the protein’s phosphorylation level. A transcription factor, BsmT, whose coding gene is located in the same tetra-cistronic operon as bsmR, was shown to directly bind to the promoter region of the operon and, through a positive regulatory loop, modulate bsmR transcription. Thus, our results revealed that the c-di-GMP signaling pathway controls biofilm formation and swimming in S. maltophilia, suggesting c-di-GMP signaling as a target in the development of novel antibacterial agents to resist this pathogen.

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Section: Introductionmentioning

confidence: 99%

BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia

Liu

Tian

Wei

et al. 2017

Sci Rep

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“…All these genes were located on the chromosome. Genes responsible for polysaccharide production ( spgM , rmlA , and rmlC ) ( Huang et al., 2006 ; Pompilio et al., 2011 ; Zhuo et al., 2014 ; Madi et al., 2016 ), quorum sensing (QS) ( rpfF , ax21 , and smoR ) ( Bahar et al., 2014 ; Devos et al., 2015 ; García et al., 2015 ; Huedo et al., 2015 ; Martínez et al., 2015 ; Ryan et al., 2015 ; Huedo et al., 2018 ), and flagella ( fleQ , flgE/G/G/K/I , flhA, fliF/I/K/M/N/O/A , and fimV ) ( Roscetto et al., 2012 ; Yang et al., 2014 ; Kang et al., 2015 ; Liu et al., 2017 ; Kim et al., 2018 ) were identified in S. maltophilia SMYN41–SMYN45 ( Flores-Treviño et al., 2019 ). Several other biofilm-related genes ( purE/D/C/I , guaA , and ravS ) were annotated in the five strains ( Kang et al., 2015 ).…”

Section: Resultsmentioning

confidence: 99%

Comparative genomics analysis of Stenotrophomonas maltophilia strains from a community

Li,

Liu,

Chen

et al. 2023

Front. Cell. Infect. Microbiol.

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BackgroundStenotrophomonas maltophilia is a multidrug-resistant (MDR) opportunistic pathogen with high resistance to most clinically used antimicrobials. The dissemination of MDR S. maltophilia and difficult treatment of its infection in clinical settings are global issues.MethodsTo provide more genetic information on S. maltophilia and find a better treatment strategy, we isolated five S. maltophilia, SMYN41–SMYN45, from a Chinese community that were subjected to antibiotic susceptibility testing, biofilm formation assay, and whole-genome sequencing. Whole-genome sequences were compared with other thirty-seven S. maltophilia sequences.ResultsThe five S. maltophilia strains had similar antibiotic resistance profiles and were resistant to β-lactams, aminoglycosides, and macrolides. They showed similar antimicrobial resistance (AMR) genes, including various efflux pumps, β-lactamase resistance genes (blaL1/2), aminoglycoside resistance genes [aac(6’), aph(3’/6)], and macrolide-resistant gene (MacB). Genome sequencing analysis revealed that SMYN41-SMYN45 belonged to sequence type 925 (ST925), ST926, ST926, ST31, and ST928, respectively, and three new STs were identified (ST925, ST926, and ST928).ConclusionThis study provides genetic information by comparing genome sequences of several S. maltophilia isolates from a community of various origins, with the aim of optimizing empirical antibiotic medication and contributing to worldwide efforts to tackle antibiotic resistance.

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“… Yang et al (2014) reported that flagellar gene expression in S. maltophilia is controlled by FleQ (Smlt2295). This transcriptional regulator, an enhancer-binding protein, is homologous to the similar master regulator in P. aeruginosa and it is the major target for the c-di-GMP produced by the wrinkly spreader phenotype (Wsp) chemosensory system pathway ( Hickman et al, 2005 ; Yang et al, 2014 ). FleQ works together with a putative ATPase, FleN, and is inhibited by binding c-di-GMP.…”

Section: Flagellamentioning

confidence: 99%

“…FleQ works together with a putative ATPase, FleN, and is inhibited by binding c-di-GMP. Inhibition of this complex and, therefore, Wsp pathway activation results in elevated expression of biofilm-associated pel , psl, and cdr operons and a reduction of flagellar gene expression ( Hickman et al, 2005 ; Hickman and Harwood, 2008 ; Yang et al, 2014 ). The situation is reversed if the concentration of c-di-GMP is low: FleQ remains unbounded, and it leads to increased expression of flagellar genes, and, therefore, the ability of bacteria to be sessile in biofilms decreases.…”

Section: Flagellamentioning

confidence: 99%

Stenotrophomonas maltophilia virulence: a current view

Mikhailovich,

Heydarov,

Zimenkov

et al. 2024

Front. Microbiol.

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Stenotrophomonas maltophilia is an opportunistic pathogen intrinsically resistant to multiple and broad-spectrum antibiotics. Although the bacterium is considered a low-virulence pathogen, it can cause various severe diseases and contributes significantly to the pathogenesis of multibacterial infections. During the COVID-19 pandemic, S. maltophilia has been recognized as one of the most common causative agents of respiratory co-infections and bacteremia in critically ill COVID-19 patients. The high ability to adapt to unfavorable environments and new habitat niches, as well as the sophisticated switching of metabolic pathways, are unique mechanisms that attract the attention of clinical researchers and experts studying the fundamental basis of virulence. In this review, we have summarized the current knowledge on the molecular aspects of S. maltophilia virulence and putative virulence factors, partially touched on interspecific bacterial interactions and iron uptake systems in the context of virulence, and have not addressed antibiotic resistance.

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Crystallization of the N-terminal regulatory domain of the enhancer-binding protein FleQ fromStenotrophomonas maltophilia

Cited by 7 publications

References 27 publications

BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia

BsmR degrades c-di-GMP to modulate biofilm formation of nosocomial pathogen Stenotrophomonas maltophilia

Comparative genomics analysis of Stenotrophomonas maltophilia strains from a community

Stenotrophomonas maltophilia virulence: a current view

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