Identification of a sensor histidine kinase (BfcK) controlling biofilm formation in Clostridium acetobutylicum

2021 ◽  
Author(s):  
Dong Liu ◽  
Shikai Ge ◽  
Zhenyu Wang ◽  
Mengting Li ◽  
Wei Zhuang ◽  
...  
Keyword(s):  
Histidine Kinase ◽  
Biofilm Formation ◽  
Clostridium Acetobutylicum ◽  
Sensor Histidine Kinase

scholarly journals Overexpression of VpsS, a Hybrid Sensor Kinase, Enhances Biofilm Formation in Vibrio cholerae

2009 ◽  
Vol 191 (16) ◽  
pp. 5147-5158 ◽  
Author(s):  
Nicholas J. Shikuma ◽  
Jiunn C. N. Fong ◽  
Lindsay S. Odell ◽  
Barrett S. Perchuk ◽  
Michael T. Laub ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Histidine Kinase ◽  
Biofilm Formation ◽  
Response Regulator ◽  
Sensor Histidine Kinase ◽  
Key Factor ◽  
Vitro Analysis ◽  
In Vitro Analysis

ABSTRACT Vibrio cholerae causes the disease cholera and inhabits aquatic environments. One key factor in the environmental survival of V. cholerae is its ability to form matrix-enclosed, surface-associated microbial communities known as biofilms. Mature biofilms rely on Vibrio polysaccharide to connect cells to each other and to a surface. We previously described a core regulatory network, which consists of two positive transcriptional regulators, VpsR and VpsT, and a negative transcriptional regulator HapR, that controls biofilm formation by regulating the expression of vps genes. In this study, we report the identification of a sensor histidine kinase, VpsS, which can control biofilm formation and activates the expression of vps genes. VpsS required the response regulator VpsR to activate vps expression. VpsS is a hybrid sensor histidine kinase that is predicted to contain both histidine kinase and response regulator domains, but it lacks a histidine phosphotransferase (HPT) domain. We determined that VpsS acts through the HPT protein LuxU, which is involved in a quorum-sensing signal transduction network in V. cholerae. In vitro analysis of phosphotransfer relationships revealed that LuxU can specifically reverse phosphotransfer to CqsS, LuxQ, and VpsS. Furthermore, mutational and phenotypic analyses revealed that VpsS requires the response regulator LuxO to activate vps expression, and LuxO positively regulates the transcription of vpsR and vpsT. The induction of vps expression via VpsS was also shown to occur independent of HapR. Thus, VpsS utilizes components of the quorum-sensing pathway to modulate biofilm formation in V. cholerae.

scholarly journals A Unique GTP-Dependent Sporulation Sensor Histidine Kinase in Bacillus anthracis

2008 ◽  
Vol 191 (3) ◽  
pp. 687-692 ◽  
Author(s):  
Francesca Scaramozzino ◽  
Andrea White ◽  
Marta Perego ◽  
James A. Hoch
Keyword(s):  
Bacillus Anthracis ◽  
Histidine Kinase ◽  
Catalytic Domain ◽  
Coiled Coil ◽  
Reverse Reaction ◽  
Forward Reaction ◽  
Critical Signal ◽  
Sensor Histidine Kinase ◽  
Virulence Plasmids ◽  
Kinase Catalytic Domain

ABSTRACT The Bacillus anthracis BA2291 gene codes for a sensor histidine kinase involved in the induction of sporulation. Genes for orthologs of the sensor domain of the BA2291 kinase exist in virulence plasmids in this organism, and these proteins, when expressed, inhibit sporulation by converting BA2291 to an apparent phosphatase of the sporulation phosphorelay. Evidence suggests that the sensor domains inhibit BA2291 by titrating its activating signal ligand. Studies with purified BA2291 revealed that this kinase is uniquely specific for GTP in the forward reaction and GDP in the reverse reaction. The G1 motif of BA2291 is highly modified from ATP-specific histidine kinases, and modeling this motif in the structure of the kinase catalytic domain suggested how guanine binds to the region. A mutation in the putative coiled-coil linker between the sensor domain and the catalytic domains was found to decrease the rate of the forward autophosphorylation reaction and not affect the reverse reaction from phosphorylated Spo0F. The results suggest that the activating ligand for BA2291 is a critical signal for sporulation and in a limited concentration in the cell. Decreasing the response to it either by slowing the forward reaction through mutation or by titration of the ligand by expressing the plasmid-encoded sensor domains switches BA2291 from an inducer to an inhibitor of the phosphorelay and sporulation.

scholarly journals Novel Family of Sensor Histidine Kinase Genes in Arabidopsis thaliana

2001 ◽  
Vol 42 (2) ◽  
pp. 231-235 ◽  
Author(s):  
Chiharu Ueguchi ◽  
Hiromi Koizumi ◽  
Tomomi Suzuki ◽  
Takeshi Mizuno
Keyword(s):  
Arabidopsis Thaliana ◽  
Histidine Kinase ◽  
Sensor Histidine Kinase

Homology modelling of a sensor histidine kinase from Aeromonas hydrophila

2009 ◽  
Vol 16 (5) ◽  
pp. 1003-1009 ◽  
Author(s):  
Mobashar Hussain Urf Turabe Fazil ◽  
Sunil Kumar ◽  
Naidu Subbarao ◽  
Haushila Prasad Pandey ◽  
Durg Vijai Singh
Keyword(s):  
Aeromonas Hydrophila ◽  
Histidine Kinase ◽  
Homology Modelling ◽  
Sensor Histidine Kinase

scholarly journals Inactivation of the ciaH Gene in Streptococcus mutans Diminishes Mutacin Production and Competence Development, Alters Sucrose-Dependent Biofilm Formation, and Reduces Stress Tolerance

2004 ◽  
Vol 72 (8) ◽  
pp. 4895-4899 ◽  
Author(s):  
Fengxia Qi ◽  
Justin Merritt ◽  
Renate Lux ◽  
Wenyuan Shi
Keyword(s):  
Stress Tolerance ◽  
Streptococcus Mutans ◽  
Histidine Kinase ◽  
Dental Plaque ◽  
Biofilm Formation ◽  
Competence Development ◽  
Clinical Isolates ◽  
Peptide Antibiotics ◽  
Kinase Gene

ABSTRACT Many clinical isolates of Streptococcus mutans produce peptide antibiotics called mutacins. Mutacin production may play an important role in the ecology of S. mutans in dental plaque. In this study, inactivation of a histidine kinase gene, ciaH, abolished mutacin production. Surprisingly, the same mutation also diminished competence development, stress tolerance, and sucrose-dependent biofilm formation.

scholarly journals Routes of phosphoryl group transfer during signal transmission and signal decay in the dimeric sensor histidine kinase ArcB

2018 ◽  
Vol 293 (34) ◽  
pp. 13214-13223 ◽  
Author(s):  
Juan L. Teran-Melo ◽  
Gabriela R. Peña-Sandoval ◽  
Hortencia Silva-Jimenez ◽  
Claudia Rodriguez ◽  
Adrián F. Alvarez ◽  
...  
Keyword(s):  
Histidine Kinase ◽  
Signal Transmission ◽  
Phosphoryl Group ◽  
Sensor Histidine Kinase ◽  
Group Transfer ◽  
Signal Decay

scholarly journals The Histidine Kinase BinK Is a Negative Regulator of Biofilm Formation and Squid Colonization

2016 ◽  
Vol 198 (19) ◽  
pp. 2596-2607 ◽  
Author(s):  
John F. Brooks ◽  
Mark J. Mandel
Keyword(s):  
Histidine Kinase ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Negative Regulator ◽  
Epithelial Tissue ◽  
Temperature Modulation ◽  
Content Type ◽  
Animal Hosts ◽  
Biofilm Development

ABSTRACTBacterial colonization of animal epithelial tissue is a dynamic process that relies on precise molecular communication. Colonization ofEuprymna scolopesbobtail squid byVibrio fischeribacteria requires bacterial aggregation in host mucus as the symbiont transitions from a planktonic lifestyle in seawater to a biofilm-associated state in the host. We have identified a gene,binK(biofilm inhibitor kinase; VF_A0360), which encodes an orphan hybrid histidine kinase that negatively regulates theV. fischerisymbiotic biofilm (Syp)in vivoandin vitro. We identifiedbinKmutants as exhibiting a colonization advantage in a global genetic screen, a phenotype that we confirmed in controlled competition experiments. Bacterial biofilm aggregates in the host are larger in strains lacking BinK, whereas overexpression of BinK suppresses biofilm formation and squid colonization. Signaling through BinK is required for temperature modulation of biofilm formation at 28°C. Furthermore, we present evidence that BinK acts upstream of SypG, the σ54-dependent transcriptional regulator of thesypbiofilm locus. The BinK effects are dependent on intact signaling in the RscS-Syp biofilm pathway. Therefore, we propose that BinK antagonizes the signal from RscS and serves as an integral component inV. fischeribiofilm regulation.IMPORTANCEBacterial lifestyle transitions underlie the colonization of animal hosts from environmental reservoirs. Formation of matrix-enclosed, surface-associated aggregates (biofilms) is common in beneficial and pathogenic associations, but investigating the genetic basis of biofilm development in live animal hosts remains a significant challenge. Using the bobtail squid light organ as a model, we analyzed putative colonization factors and identified a histidine kinase that negatively regulates biofilm formation at the host interface. This work reveals a novelin vivobiofilm regulator that influences the transition of bacteria from their planktonic state in seawater to tight aggregates of cells in the host. The study enriches our understanding of biofilm regulation and beneficial colonization by an animal's microbiome.

scholarly journals The Two-Component Signal Transduction System VxrAB Positively Regulates Vibrio cholerae Biofilm Formation

2017 ◽  
Vol 199 (18) ◽  
Author(s):  
Jennifer K. Teschler ◽  
Andrew T. Cheng ◽  
Fitnat H. Yildiz
Keyword(s):  
Signal Transduction ◽  
Vibrio Cholerae ◽  
Histidine Kinase ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Response Regulator ◽  
Systematic Analysis ◽  
Content Type ◽  
Two Component ◽  
Two Component Signal Transduction

ABSTRACT Two-component signal transduction systems (TCSs), typically composed of a sensor histidine kinase (HK) and a response regulator (RR), are the primary mechanism by which pathogenic bacteria sense and respond to extracellular signals. The pathogenic bacterium Vibrio cholerae is no exception and harbors 52 RR genes. Using in-frame deletion mutants of each RR gene, we performed a systematic analysis of their role in V. cholerae biofilm formation. We determined that 7 RRs impacted the expression of an essential biofilm gene and found that the recently characterized RR, VxrB, regulates the expression of key structural and regulatory biofilm genes in V. cholerae. vxrB is part of a 5-gene operon, which contains the cognate HK vxrA and three genes of unknown function. Strains carrying ΔvxrA and ΔvxrB mutations are deficient in biofilm formation, while the ΔvxrC mutation enhances biofilm formation. The overexpression of VxrB led to a decrease in motility. We also observed a small but reproducible effect of the absence of VxrB on the levels of cyclic di-GMP (c-di-GMP). Our work reveals a new function for the Vxr TCS as a regulator of biofilm formation and suggests that this regulation may act through key biofilm regulators and the modulation of cellular c-di-GMP levels. IMPORTANCE Biofilms play an important role in the Vibrio cholerae life cycle, providing protection from environmental stresses and contributing to the transmission of V. cholerae to the human host. V. cholerae can utilize two-component systems (TCS), composed of a histidine kinase (HK) and a response regulator (RR), to regulate biofilm formation in response to external cues. We performed a systematic analysis of V. cholerae RRs and identified a new regulator of biofilm formation, VxrB. We demonstrated that the VxrAB TCS is essential for robust biofilm formation and that this system may regulate biofilm formation via its regulation of key biofilm regulators and cyclic di-GMP levels. This research furthers our understanding of the role that TCSs play in the regulation of V. cholerae biofilm formation.

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