Role of Two-component Systems in Cold Tolerance ofClostridium Botulinum

Bacteria depend on two-component systems to detect and respond to threats. Simple pathways comprise a single sensor kinase (SK) that detects a signal and activates a response regulator protein to mediate an appropriate output. These simple pathways with only a single SK are not well suited to making complex decisions where multiple different stimuli need to be evaluated. A recently emerging theme is the existence of multikinase networks (MKNs) where multiple SKs collaborate to detect and integrate numerous different signals to regulate a major lifestyle switch, e.g., between virulence, sporulation, biofilm formation, and cell division. In this review, the role of MKNs and the phosphosignaling mechanisms underpinning their signal integration and decision making are explored.

Download Full-text

The Role of Two-Component Systems in Ethylene Perception

Biology and Biotechnology of the Plant Hormone Ethylene II ◽

10.1007/978-94-011-4453-7_12 ◽

1999 ◽

pp. 59-64

Author(s):

R. L. Gamble ◽

M. L. Coonfield ◽

M. D. Randlett ◽

G. E. Schaller

Keyword(s):

Component Systems ◽

Two Component ◽

Two Component Systems

Download Full-text

Role of two-component systems in the virulence of Streptococcus pneumoniae

Journal of Medical Microbiology ◽

10.1099/jmm.0.46423-0 ◽

2006 ◽

Vol 55 (4) ◽

pp. 355-363 ◽

Cited By ~ 41

Author(s):

G. K. Paterson ◽

C. E. Blue ◽

T. J. Mitchell

Keyword(s):

Streptococcus Pneumoniae ◽

Cellular Response ◽

Fluorescence Induction ◽

Environmental Response ◽

Human Pathogen ◽

Component Systems ◽

Two Component ◽

Two Component Systems ◽

Insight Into

Understanding of how the human pathogen Streptococcus pneumoniae perceives and responds to its environment in the host offers insight into the pathogenesis of disease caused by this important bacterium and the potential for improved interventions. A central role in this environmental response is played by two-component systems (TCSs), which both sense the environment and drive the cellular response. Molecular advances in the form of genome sequencing, signature-tagged mutagenesis, differential fluorescence induction and microarray analysis have yielded considerable progress in the study of these systems in S. pneumoniae. These recent advances are discussed here, focusing in particular on the role of TCSs in the virulence of S. pneumoniae.

Download Full-text

Polymyxin Resistance ofPseudomonas aeruginosa phoQMutants Is Dependent on Additional Two-Component Regulatory Systems

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.02353-12 ◽

2013 ◽

Vol 57 (5) ◽

pp. 2204-2215 ◽

Cited By ~ 56

Author(s):

Alina D. Gutu ◽

Nicole Sgambati ◽

Pnina Strasbourger ◽

Mark K. Brannon ◽

Michael A. Jacobs ◽

...

Keyword(s):

Lipid A ◽

Regulatory System ◽

Content Type ◽

Regulatory Systems ◽

Clinical Resistance ◽

Component Systems ◽

Two Component ◽

Two Component Systems ◽

High Level

ABSTRACTPseudomonas aeruginosacan develop resistance to polymyxin as a consequence of mutations in the PhoPQ regulatory system, mediated by covalent lipid A modification. Transposon mutagenesis of a polymyxin-resistantphoQmutant defined 41 novel loci required for resistance, including two regulatory systems, ColRS and CprRS. Deletion of thecolRSgenes, individually or in tandem, abrogated the polymyxin resistance of a ΔphoQmutant, as did individual or tandem deletion ofcprRS. Individual deletion ofcolRorcolSin a ΔphoQmutant also suppressed 4-amino-l-arabinose addition to lipid A, consistent with the known role of this modification in polymyxin resistance. Surprisingly, tandem deletion ofcolRSorcprRSin the ΔphoQmutant or individual deletion ofcprRorcprSfailed to suppress 4-amino-l-arabinose addition to lipid A, indicating that this modification alone is not sufficient for PhoPQ-mediated polymyxin resistance inP. aeruginosa. Episomal expression ofcolRSorcprRSin tandem or ofcprRindividually complemented the Pm resistance phenotype in the ΔphoQmutant, while episomal expression ofcolR,colS, orcprSindividually did not. Highly polymyxin-resistantphoQmutants ofP. aeruginosaisolated from polymyxin-treated cystic fibrosis patients harbored mutant alleles ofcolRSandcprS; when expressed in a ΔphoQbackground, these mutant alleles enhanced polymyxin resistance. These results define ColRS and CprRS as two-component systems regulating polymyxin resistance inP. aeruginosa, indicate that addition of 4-amino-l-arabinose to lipid A is not the only PhoPQ-regulated biochemical mechanism required for resistance, and demonstrate thatcolRSandcprSmutations can contribute to high-level clinical resistance.

Download Full-text