Faculty Opinions recommendation of Direct interaction between sensor kinase proteins mediates acute and chronic disease phenotypes in a bacterial pathogen.

2009 ◽  
Author(s):  
Fergal O'Gara
Keyword(s):  
Chronic Disease ◽  
Bacterial Pathogen ◽  
Direct Interaction ◽  
Sensor Kinase ◽  
Disease Phenotypes

scholarly journals Direct interaction between sensor kinase proteins mediates acute and chronic disease phenotypes in a bacterial pathogen

2009 ◽  
Vol 23 (2) ◽  
pp. 249-259 ◽  
Author(s):  
A. L. Goodman ◽  
M. Merighi ◽  
M. Hyodo ◽  
I. Ventre ◽  
A. Filloux ◽  
...  
Keyword(s):  
Chronic Disease ◽  
Bacterial Pathogen ◽  
Direct Interaction ◽  
Sensor Kinase ◽  
Disease Phenotypes

scholarly journals Role for GrgA in Regulation of σ28-Dependent Transcription in the Obligate Intracellular Bacterial PathogenChlamydia trachomatis

2018 ◽  
Vol 200 (20) ◽  
Author(s):  
Malhar Desai ◽  
Wurihan Wurihan ◽  
Rong Di ◽  
Joseph D. Fondell ◽  
Bryce E. Nickels ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Chlamydia Trachomatis ◽  
Sigma Factor ◽  
Bacterial Pathogen ◽  
Direct Interaction ◽  
Developmental Cycle ◽  
Content Type ◽  
Sexually Transmitted ◽  
Obligate Intracellular ◽  
Specific Transcription Factor

ABSTRACTThe obligate intracellular bacterial pathogenChlamydia trachomatishas a unique developmental cycle consisting of two contrasting cellular forms. Whereas the primaryChlamydiasigma factor, σ66, is involved in the expression of the majority of chlamydial genes throughout the developmental cycle, expression of several late genes requires the alternative sigma factor, σ28. In prior work, we identified GrgA as aChlamydia-specific transcription factor that activates σ66-dependent transcription by binding DNA and interacting with a nonconserved region (NCR) of σ66. Here, we extend these findings by showing GrgA can also activate σ28-dependent transcription through direct interaction with σ28. We measure the binding affinity of GrgA for both σ66and σ28, and we identify regions of GrgA important for σ28-dependent transcription. Similar to results obtained with σ66, we find that GrgA's interaction with σ28involves an NCR located upstream of conserved region 2 of σ28. Our findings suggest that GrgA is an important regulator of both σ66- and σ28-dependent transcription inC. trachomatisand further highlight NCRs of bacterial RNA polymerase as targets for regulatory factors unique to particular organisms.IMPORTANCEChlamydia trachomatisis the number one sexually transmitted bacterial pathogen worldwide. A substantial proportion ofC. trachomatis-infected women develop infertility, pelvic inflammatory syndrome, and other serious complications.C. trachomatisis also a leading infectious cause of blindness in underdeveloped countries. The pathogen has a unique developmental cycle that is transcriptionally regulated. The discovery of an expanded role for theChlamydia-specific transcription factor GrgA helps us understand the progression of the chlamydial developmental cycle.

scholarly journals A potential role for GrgA in regulation of σ28-dependent transcription in the obligate intracellular bacterial pathogen Chlamydia trachomatis

2018 ◽  
Author(s):  
Malhar Desai ◽  
Wurihan Wurihan ◽  
Rong Di ◽  
Joseph D. Fondell ◽  
Bryce E. Nickels ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Sigma Factor ◽  
Bacterial Pathogen ◽  
Direct Interaction ◽  
Developmental Cycle ◽  
Sexually Transmitted ◽  
Obligate Intracellular ◽  
Bacterial Rna ◽  
Important Regulator ◽  
Conserved Region

ABSTRACTThe sexually transmitted obligate intracellular bacterial pathogen Chlamydia trachomatis has a unique developmental cycle consisting of two contrasting cellular forms. Whereas the primary Chlamydia sigma factor, σ66, is involved in the expression of the majority of chlamydial genes throughout the developmental cycle, expression of several late genes requires the alternative sigma factor σ28. In prior work we identified GrgA as a Chlamydia-specific transcription factor that activates σ66-dependent transcription by binding DNA and interacting with a non-conserved region (NCR) of σ66. Here, we extend these findings by showing GrgA can also activate σ28-dependent transcription through direct interaction with σ28. We measure the binding affinity of GrgA for both σ66and σ28, and we identify regions of GrgA important for σ28-dependent transcription. Similar to results obtained with σ66, we find that GrgA’s interaction with σ28 involves a NCR located upstream of conserved region 2 of σ28. Our findings suggest GrgA is an important regulator of both σ66- and σ28-dependent transcription in C. trachomatis and further highlight NCRs of bacterial RNA polymerase as targets for regulatory factors unique to particular organisms.

scholarly journals The Sensor Kinase QseC Regulates the Unlinked PmrA Response Regulator and Downstream Gene Expression in Francisella

2020 ◽  
Vol 202 (21) ◽  
Author(s):  
Ky Van Hoang ◽  
James Fitch ◽  
Peter White ◽  
Nrusingh P. Mohapatra ◽  
John S. Gunn
Keyword(s):  
Francisella Tularensis ◽  
Response Regulator ◽  
Phosphorylation Site ◽  
Bacterial Pathogen ◽  
Sensor Kinase ◽  
Gram Negative ◽  
Content Type ◽  
Environmental Signals ◽  
Two Component ◽  
Sense And Respond

ABSTRACT The facultative intracellular bacterial pathogen Francisella tularensis is the causative agent of tularemia in humans and animals. Gram-negative bacteria utilize two-component regulatory systems (TCS) to sense and respond to their changing environment. No classical, tandemly arranged sensor kinase and response regulator TCS genes exist in the human virulent Francisella tularensis subsp. tularensis, but orphaned members are present. PmrA is an orphan response regulator responsible for intramacrophage growth and virulence; however, the regulation of PmrA activity is not understood. We and others have shown that PmrA represses the expression of priM, described to encode an antivirulence determinant. By screening a mutant library for increased priM promoter activity, we identified the sensor kinase homolog QseC as an upstream regulator of priM expression, and this regulation is in part dependent upon the aspartate phosphorylation site of PmrA (D51). Several examined environmental signals, including epinephrine, which is reported to activate QseC in other bacteria, do not affect priM expression in a manner dependent on PmrA. Intramacrophage survival assays also question the finding that PriM is an antivirulence factor. Thus, these data suggest that the PmrA-regulated gene priM is modulated by the QseC-PmrA (QseB) TCS in Francisella. IMPORTANCE The disease tularemia is caused by the highly infectious Gram-negative pathogen Francisella tularensis. This bacterium encodes few regulatory factors (e.g., two-component systems [TCS]). PmrA, required for intramacrophage survival and virulence in the mouse model, is encoded by an orphan TCS response regulator gene. It is unclear how PmrA is responsive to environmental signals to regulate loci, including the PmrA-repressed gene priM. We identify an orphan sensor kinase (QseC) that is required for priM repression and further explore both environmental signals that might regulate the QseC-PmrA TCS and the function of PriM.

scholarly journals Hybrid sensor kinase PA1611 inPseudomonas aeruginosaregulates transitions between acute and chronic infection through direct interaction with RetS

2013 ◽  
Vol 88 (4) ◽  
pp. 784-797 ◽  
Author(s):  
Weina Kong ◽  
Lin Chen ◽  
Jieqiong Zhao ◽  
Tuo Shen ◽  
Michael G. Surette ◽  
...  
Keyword(s):  
Chronic Infection ◽  
Direct Interaction ◽  
Sensor Kinase

scholarly journals Site-Specific Mutation of the Sensor Kinase GraS in Staphylococcus aureus Alters the Adaptive Response to Distinct Cationic Antimicrobial Peptides

2014 ◽  
Vol 82 (12) ◽  
pp. 5336-5345 ◽  
Author(s):  
Ambrose L. Cheung ◽  
Arnold S. Bayer ◽  
Michael R. Yeaman ◽  
Yan Q. Xiong ◽  
Alan J. Waring ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Peptides ◽  
Target Genes ◽  
Regulatory System ◽  
Direct Interaction ◽  
Sensor Kinase ◽  
Target Tissue ◽  
Cationic Antimicrobial Peptides ◽  
Content Type

ABSTRACTTheStaphylococcus aureustwo-component regulatory system, GraRS, is involved in resistance to killing by distinct host defense cationic antimicrobial peptides (HD-CAPs). It is believed to regulate downstream target genes such asmprFanddltABCDto modify theS. aureussurface charge. However, the detailed mechanism(s) by which the histidine kinase, GraS, senses specific HD-CAPs is not well defined. Here, we studied a well-characterized clinical methicillin-resistantS. aureus(MRSA) strain (MW2), its isogenicgraSdeletion mutant (ΔgraSstrain), a nonameric extracellular loop mutant (ΔEL strain), and four residue-specific ΔEL mutants (D37A, P39A, P39S, and D35G D37G D41G strains). The ΔgraSand ΔEL strains were unable to inducemprFanddltAexpression and, in turn, demonstrated significantly increased susceptibilities to daptomycin, polymyxin B, and two prototypical HD-CAPs (hNP-1 and RP-1). Further, P39A, P39S, and D35G-D37G-D41G ΔEL mutations correlated with moderate increases in HD-CAP susceptibility. Reductions ofmprFanddltAinduction by PMB were also found in the ΔEL mutants, suggesting these residues are pivotal to appropriate activation of the GraS sensor kinase. Importantly, a synthetic exogenous soluble EL mimic of GraS protected the parental MW2 strain against hNP-1- and RP-1-mediated killing, suggesting a direct interaction of the EL with HD-CAPs in GraS activation.In vivo, the ΔgraSand ΔEL strains displayed dramatic reductions in achieved target tissue MRSA counts in an endocarditis model. Taken together, our results provide new insights into potential roles of GraS inS. aureussensing of HD-CAPs to induce adaptive survival responses to these molecules.

Nutrient-regulated gene expression in eukaryotes

2006 ◽  
Vol 73 ◽  
pp. 85-96 ◽  
Author(s):  
Richard J. Reece ◽  
Laila Beynon ◽  
Stacey Holden ◽  
Amanda D. Hughes ◽  
Karine Rébora ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcriptional Control ◽  
Direct Interaction ◽  
Signalling Pathways ◽  
A Cell ◽  
One Step ◽  
Higher Eukaryotes ◽  
Regulated Gene Expression

The recognition of changes in environmental conditions, and the ability to adapt to these changes, is essential for the viability of cells. There are numerous well characterized systems by which the presence or absence of an individual metabolite may be recognized by a cell. However, the recognition of a metabolite is just one step in a process that often results in changes in the expression of whole sets of genes required to respond to that metabolite. In higher eukaryotes, the signalling pathway between metabolite recognition and transcriptional control can be complex. Recent evidence from the relatively simple eukaryote yeast suggests that complex signalling pathways may be circumvented through the direct interaction between individual metabolites and regulators of RNA polymerase II-mediated transcription. Biochemical and structural analyses are beginning to unravel these elegant genetic control elements.

Demonstration of a direct interaction between a colonic divalent cation receptor and the basolateral Na−H exchanger

2001 ◽  
Vol 120 (5) ◽  
pp. A529-A530
Author(s):  
P GEIBEL ◽  
M OREILLY ◽  
H VIEWEGER ◽  
K SIEBERT ◽  
N OBREIN ◽  
...  
Keyword(s):  
Divalent Cation ◽  
Direct Interaction ◽  
Cation Receptor

Chronic Disease of the Liver in Young Women: An Evaluation of Patients with a Negative Clot Test for Lupus Erythematosus

1962 ◽  
Vol 43 (5) ◽  
pp. 532-538 ◽  
Author(s):  
Clarence P. Alfrey ◽  
Lloyd G. Bartholomew ◽  
James C. Cain ◽  
Archie H. Baggbnstoss
Keyword(s):  
Chronic Disease ◽  
Young Women ◽  
Lupus Erythematosus
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