Crystallization of and preliminary X-ray data for the negative regulator (AmiC) of the amidase operon of Pseudomonas aeruginosa

1991 ◽  
Vol 222 (4) ◽  
pp. 869-871 ◽  
Author(s):  
Stuart A. Wilson ◽  
Naomi E. Chayen ◽  
Andrew M. Hemmings ◽  
Robert E. Drew ◽  
Laurence H. Pearl
2004 ◽  
Vol 186 (9) ◽  
pp. 2880-2890 ◽  
Author(s):  
Isabelle Vallet ◽  
Stephen P. Diggle ◽  
Rachael E. Stacey ◽  
Miguel Cámara ◽  
Isabelle Ventre ◽  
...  

ABSTRACT Pseudomonas aeruginosa is an opportunistic bacterial pathogen which poses a major threat to long-term-hospitalized patients and individuals with cystic fibrosis. The capacity of P. aeruginosa to form biofilms is an important requirement for chronic colonization of human tissues and for persistence in implanted medical devices. Various stages of biofilm formation by this organism are mediated by extracellular appendages, such as type IV pili and flagella. Recently, we identified three P. aeruginosa gene clusters that were termed cup (chaperone-usher pathway) based on their sequence relatedness to the chaperone-usher fimbrial assembly pathway in other bacteria. The cupA gene cluster, but not the cupB or cupC cluster, is required for biofilm formation on abiotic surfaces. In this study, we identified a gene (mvaT) encoding a negative regulator of cupA expression. Such regulatory control was confirmed by several approaches, including lacZ transcriptional fusions, Northern blotting, and transcriptional profiling using DNA microarrays. MvaT also represses the expression of the cupB and cupC genes, although the extent of the regulatory effect is not as pronounced as with cupA. Consistent with this finding, mvaT mutants exhibit enhanced biofilm formation. Although the P. aeruginosa genome contains a highly homologous gene, mvaU, the repression of cupA genes is MvaT specific. Thus, MvaT appears to be an important regulatory component within a complex network that controls biofilm formation and maturation in P. aeruginosa.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yanyan Li ◽  
Zhenling Wang ◽  
Xiaoxiao Liu ◽  
Jianying Tang ◽  
Bin Peng ◽  
...  
Keyword(s):  

2009 ◽  
Vol 191 (7) ◽  
pp. 2285-2295 ◽  
Author(s):  
F. Heath Damron ◽  
Dongru Qiu ◽  
Hongwei D. Yu

ABSTRACT Mucoidy, or overproduction of the exopolysaccharide known as alginate, in Pseudomonas aeruginosa is a poor prognosticator for lung infections in cystic fibrosis. Mutation of the anti-σ factor MucA is a well-accepted mechanism for mucoid conversion. However, certain clinical mucoid strains of P. aeruginosa have a wild-type (wt) mucA. Here, we describe a loss-of-function mutation in kinB that causes overproduction of alginate in the wt mucA strain PAO1. KinB is the cognate histidine kinase for the transcriptional activator AlgB. Increased alginate production due to inactivation of kinB was correlated with high expression at the alginate-related promoters P algU and P algD . Deletion of alternative σ factor RpoN (σ54) or the response regulator AlgB in kinB mutants decreased alginate production to wt nonmucoid levels. Mucoidy was restored in the kinB algB double mutant by expression of wt AlgB or phosphorylation-defective AlgB.D59N, indicating that phosphorylation of AlgB was not required for alginate overproduction when kinB was inactivated. The inactivation of the DegS-like protease AlgW in the kinB mutant caused loss of alginate production and an accumulation of the hemagglutinin (HA)-tagged MucA. Furthermore, we observed that the kinB mutation increased the rate of HA-MucA degradation. Our results also indicate that AlgW-mediated MucA degradation required algB and rpoN in the kinB mutant. Collectively, these studies indicate that KinB is a negative regulator of alginate production in wt mucA strain PAO1.


2021 ◽  
Author(s):  
Davood Gheidari ◽  
Morteza Mehrdad ◽  
Saloomeh Maleki ◽  
Samanesadat Hosseini

Abstract With the increase of general knowledge and the advancement of science and technology, antibacterial substances were used more than antibiotics. In our current study, the antibacterial virtues of CFO/BiOI nanocomposite were investigated due to its high importance on Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa and Bacillus cereus. MIC, MBC , Disk Diffusion and IC50 tests Cefalotin (CF), Amoxicillin (AMX), Gentamicin (GM), Trimethoprim-sulphamethoxazole (SXT) and Ceftriaxone (CRO) antibiotics in concentration 30W, 10i, 10t , 25h and 30 were used to find the antibacterial properties of the synthesized nanocomposite, respectively. For the synthesis of nanocomposites polyethylene glycol (PEG) and sulfonic acid was used as a solvent. It is noteworthy that the synthesis was performed by heat dissolution method without the presence of surfactant. Also, various techniques such as X-Ray Diffraction(XRD), Scanning Electron Microscope (SEM), High resolution mapping and Energy Dispersive X-ray spectroscopy (EDAX) have been used to determine the properties of produced nanocomposites. SEM test results showed that the formed nanoparticles were globular and their size was limited area of 22 to 34 nm. The results showed CFO / BiOI nanocomposite exhibits strong significant biological activity against Bacillus cereus. The results of MBC (Minimum Bactericidal Concentration) and MIC (Minimum Inhibition Concentration) tests for CFO/BiOI nanocomposites on bacteria were examined in the range of 0.12-0.48 mg/ml and 0.06 to 0.24 mg/ml respectively. According to the results, the minimum IC50 value was determined at a concentration of 0.061 mg/ml. On the other hand, the most resisting and susceptible bacteria in this method were Pseudomonas aeruginosa and Bacillus cereus, respectively. These findings are identical to those of a prior study on CoFe2O4 nanoparticles antibacterial properties. MBC of the nanocomposites, 50 µl from all the tubes that showed no obvious bacterial growth were distributed on BHI agar plates and incubated for 24 h at 37 ◦C. The MBC endpoint is defined as the lowest concentration which killed 98% of the bacterial population.


2013 ◽  
Vol 135 (28) ◽  
pp. 10318-10321 ◽  
Author(s):  
Siseth Martínez-Caballero ◽  
Mijoon Lee ◽  
Cecilia Artola-Recolons ◽  
César Carrasco-López ◽  
Dusan Hesek ◽  
...  

1989 ◽  
Vol 205 (3) ◽  
pp. 617-618 ◽  
Author(s):  
John J. Stezowski ◽  
Helmut Görisch ◽  
Zbigniew Dauter ◽  
Michael Rupp ◽  
Andrea Hoh ◽  
...  

1999 ◽  
Vol 55 (2) ◽  
pp. 539-541
Author(s):  
Palangpon Kongsaeree ◽  
Jun Liang ◽  
Roy A. Jensen ◽  
Jon Clardy

The title protein has been crystallized in a new crystal form. The crystals belong to the cubic space group P4132 (or P4332) with unit-cell dimensions a = b = c = 126.1 Å at 100 K and typically diffract beyond 1.6 Å at the Cornell High Energy Synchotron Source (CHESS) A1 beamline.


2018 ◽  
Vol 13 (4) ◽  
pp. 1934578X1801300
Author(s):  
Daniyar Sadyrbekov ◽  
Timur Saliev ◽  
Yuri Gatilov ◽  
Ivan Kulakov ◽  
Roza Seidakhmetova ◽  
...  

A cyclopropane derivative of limonene, (1 S, 4 S, 6 R)-7,7-dichloro-4-[(1 S)-2,2-dichloro-1-methylcyclopropyl]-1-methylbicyclo [4.1.0] heptane (compound 2), was synthesized and its structure was determined by NMR and X-ray crystallographic methods. In addition, an antimicrobial activity of the compound against Gram-positive ( Staphylococcus aureus, Bacillus subtilis) and Gram-negative ( Escherichia coli, Pseudomonas aeruginosa) bacterial strains was also scrutinized.


2011 ◽  
Vol 80 (1) ◽  
pp. 100-109 ◽  
Author(s):  
Tania Véliz Rodriguez ◽  
Federica Moalli ◽  
Nadia Polentarutti ◽  
Moira Paroni ◽  
Eduardo Bonavita ◽  
...  

ABSTRACTToll interleukin-1 receptor (IL-1R) 8 (TIR8), also known as single Ig IL-1 receptor (IL-R)-related molecule, or SIGIRR, is a member of the IL-1R-like family, primarily expressed by epithelial cells. Current evidence suggests that TIR8 plays a nonredundant role as a negative regulatorin vivounder different inflammatory conditions that are dependent on IL-R and Toll-like receptor (TLR) activation. In the present study, we examined the role of TIR8 in innate resistance to acute lung infections caused byPseudomonas aeruginosa, a Gram-negative pathogen responsible for life-threatening infections in immunocompromised individuals and cystic fibrosis patients. We show that Tir8 deficiency in mice was associated with increased susceptibility to acuteP. aeruginosainfection, in terms of mortality and bacterial load, and to exacerbated local and systemic production of proinflammatory cytokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], IL-1β, and IL-6) and chemokines (CXCL1, CXCL2, and CCL2). It has been reported that host defense againstP. aeruginosaacute lung infection can be improved by blocking IL-1 since exaggerated IL-1β production may be harmful for the host in this infection. In agreement with these data, IL-1RI deficiency rescues the phenotype observed in Tir8-deficient mice: in Tir8−/−IL-1RI−/−double knockout mice we observed higher survival rates, enhanced bacterial clearance, and reduced levels of local and systemic cytokine and chemokine levels than in Tir8-deficient mice. These results suggest that TIR8 has a nonredundant effect in modulating the inflammation caused byP. aeruginosa, in particular, by negatively regulating IL-1RI signaling, which plays a major role in the pathogenesis of this infectious disease.


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