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Microscopy-based Assays for High-throughput Screening of Host Factors Involved in Brucella Infection of Hela Cells
Published on: August 5, 2016
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LOV Histidine Kinase Modulates the General Stress Response System and Affects the virB Operon Expression in Brucella
Gabriela Sycz1, Mariela Carmen Carrica1, Tong-Seung Tseng2
1Laboratorio de Inmunología y Microbiología Molecular, Fundación Instituto Leloir (IIBBA-CONICET), Buenos Aires, Argentina.
Plos One
|May 21, 2015
Summary
Brucella
Area of Science:
- Microbiology
- Molecular Biology
- Bacterial Pathogenesis
Background:
- Brucella causes brucellosis, a zoonotic disease.
- Intracellular survival of Brucella depends on adapting to host conditions.
- A light-sensing histidine kinase, LOVHK, regulates Brucella virulence.
Purpose of the Study:
- Investigate the intracellular signaling pathway of the LOVHK sensor in Brucella.
- Elucidate the role of LOVHK in bacterial stress response and virulence gene expression.
Main Methods:
- Bacterial two-hybrid assays to study protein interactions.
- Phosphotransfer experiments to analyze signaling dynamics.
- Genetic approaches to assess gene expression changes.
Main Results:
- LOVHK interacts with response regulators PhyR and LovR, forming a two-component system.
- LOVHK activates the General Stress Response (GSR) via PhyR.
- LovR acts as a phosphate sink for LOVHK, modulating its activity.
- Absence of LOVHK leads to down-regulation of the virB operon.
Conclusions:
- LOVHK positively regulates the GSR system in vivo.
- LOVHK influences the expression of the virB operon in Brucella.
- The identified regulatory network may be conserved in other microorganisms.
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