A molecular mechanism for how sigma factor AlgT and transcriptional regulator AmrZ inhibit twitching motility in <i>Pseudomonas aeruginosa</i>

Xu, Anming; Zhang, Miaokun; Du, Wei; Wang, Di; Zhang, Luyan

doi:10.1111/1462-2920.14985

Cited by 13 publications

(15 citation statements)

References 69 publications

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“…Thus, it is possible that the biofilm enhancement observed in the Pf4*-T condition was partly due to AmrZ transcriptional activity on pelB, algD and pslB, and of FleQ on pel operon. In addition, the AmrZ-repressed pilA gene [80] was strongly downregulated (Figure 4A), in line with the reduced twitching motility (as shown in Figure 2E), comforting a possible AmrZ activity. However, while significant, this two-fold increased expression of both amrZ and fleQ remains modest, suggesting that other mechanisms would be involved in the observed biofilm alterations in response to Pf4 treatment.…”

Section: Increased Matrix-encoding Genes Expression and C-di-gmp Production In Response To Pf4 Variant Infectionsupporting

confidence: 69%

Activation of the Cell Wall Stress Response in Pseudomonas aeruginosa Infected by a Pf4 Phage Variant

et al. 2020

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Pseudomonas aeruginosa PAO1 has an integrated Pf4 prophage in its genome, encoding a relatively well-characterized filamentous phage, which contributes to the bacterial biofilm organization and maturation. Pf4 variants are considered as superinfectives when they can re-infect and kill the prophage-carrying host. Herein, the response of P. aeruginosa H103 to Pf4 variant infection was investigated. This phage variant caused partial lysis of the bacterial population and modulated H103 physiology. We show by confocal laser scanning microscopy that a Pf4 variant-infection altered P. aeruginosa H103 biofilm architecture either in static or dynamic conditions. Interestingly, in the latter condition, numerous cells displayed a filamentous morphology, suggesting a link between this phenotype and flow-related forces. In addition, Pf4 variant-infection resulted in cell envelope stress response, mostly mediated by the AlgU and SigX extracytoplasmic function sigma factors (ECFσ). AlgU and SigX involvement may account, at least partly, for the enhanced expression level of genes involved in the biosynthesis pathways of two matrix exopolysaccharides (Pel and alginates) and bis-(3’-5’)-cyclic dimeric guanosine monophosphate (c-di-GMP) metabolism.

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Section: Increased Matrix-encoding Genes Expression and C-di-gmp Production In Response To Pf4 Variant Infectionsupporting

confidence: 69%

Activation of the Cell Wall Stress Response in Pseudomonas aeruginosa Infected by a Pf4 Phage Variant

et al. 2020

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“…Nonetheless, most of CF isolates exhibit rpoN mutations, provoking the loss of both pili and flagella [20,274,275]. Recently, AlgT and AmrZ were shown to be involved in pilA gene repression, thereby inhibiting pili formation and twitching motility [276].…”

Section: Lack Of Motility and Non-flagellated Non-piliated Phenotypementioning

confidence: 99%

Pseudomonas aeruginosa: An Audacious Pathogen with an Adaptable Arsenal of Virulence Factors

Jurado‐Martín

Sainz-Mejías

McClean

2021

IJMS

319

266

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Pseudomonas aeruginosa is a dominant pathogen in people with cystic fibrosis (CF) contributing to morbidity and mortality. Its tremendous ability to adapt greatly facilitates its capacity to cause chronic infections. The adaptability and flexibility of the pathogen are afforded by the extensive number of virulence factors it has at its disposal, providing P. aeruginosa with the facility to tailor its response against the different stressors in the environment. A deep understanding of these virulence mechanisms is crucial for the design of therapeutic strategies and vaccines against this multi-resistant pathogen. Therefore, this review describes the main virulence factors of P. aeruginosa and the adaptations it undergoes to persist in hostile environments such as the CF respiratory tract. The very large P. aeruginosa genome (5 to 7 MB) contributes considerably to its adaptive capacity; consequently, genomic studies have provided significant insights into elucidating P. aeruginosa evolution and its interactions with the host throughout the course of infection.

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“…AmrZ was shown to regulate genes important for P. aeruginosa virulence, including type IV pili, extracellular polysaccharides, and the flagellum (34). It particularly influences genes required for alginate production and twitching-motility (34, 62–64). Within the c-di-GMP network of P. aeruginosa , AmrZ activates transcription of 14 genes and represses 10 genes encoding GGDEF/EAL-domain proteins ((34), Table 3).…”

Section: Resultsmentioning

confidence: 99%

ThePseudomonas aeruginosaphosphodiesterase genenbdAis transcriptionally regulated by RpoS and AmrZ

Gerbracht

Zehner

Frankenberg‐Dinkel

2021

Preprint

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Pseudomonas aeruginosa is an opportunistic pathogen causing serious infections in immune compromised persons. These infections are difficult to erase with antibiotics, due to the formation of biofilms. The biofilm lifecycle is regulated by the second messenger molecule c-di-GMP (bis-3,5-cyclic di-guanosine monophosphate). P. aeruginosa encodes 40 genes for enzymes presumably involved in the biosynthesis and degradation of c-di-GMP. A tight regulation of expression, subcellular localized function and protein interactions control the activity of these enzymes. In this work we elucidated the transcriptional regulation of the gene encoding the membrane-bound phosphodiesterase NbdA. We previously reported a transcriptional and posttranslational role of nitric oxide (NO) on nbdA and its involvement in biofilm dispersal. NO is released from macrophages during infections but can also be produced by P. aeruginosa itself during anaerobic denitrification. Recently however, contradictory results about the role of NbdA within NO-induced biofilm dispersal were published. Therefore, the transcriptional regulation of nbdA was reevaluated to obtain insights into this discrepancy. Determination of the transcriptional start site of nbdA by 5'-RACE and subsequent identification of the promoter region revealed a shortened open reading frame (ORF) in contrast to the annotated one. In addition, putative binding sites for RpoS and AmrZ were discovered in the newly defined promoter region. Employing chromosomally integrated transcriptional lacZ reporter gene fusions demonstrated a RpoS-dependent activation and AmrZ repression of nbdA transcription. In order to investigate the impact of NO on nbdA transcription, conditions mimicking exogenous and endogenous NO were applied. While neither exogenous nor endogenous NO had an influence on nbdA promoter activity, deletion of the nitrite reductase gene nirS strongly increased nbdA transcription independently of its enzymatic activity during denitrification. The latter supports a role of NirS in P. aeruginosa apart from its enzymatic function.

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A molecular mechanism for how sigma factor AlgT and transcriptional regulator AmrZ inhibit twitching motility in Pseudomonas aeruginosa

Cited by 13 publications

References 69 publications

Activation of the Cell Wall Stress Response in Pseudomonas aeruginosa Infected by a Pf4 Phage Variant

Activation of the Cell Wall Stress Response in Pseudomonas aeruginosa Infected by a Pf4 Phage Variant

Pseudomonas aeruginosa: An Audacious Pathogen with an Adaptable Arsenal of Virulence Factors

ThePseudomonas aeruginosaphosphodiesterase genenbdAis transcriptionally regulated by RpoS and AmrZ

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