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Updated: May 6, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
Published on: June 25, 2015
A tetracycline-inducible expression vector for Streptococcus agalactiae allowing controllable gene expression.
Marie-Frédérique Lartigue1, Philippe Bouloc2
1Institut de Génétique et Microbiologie, CNRS/UMR 8621, Centre scientifique d'Orsay, Université Paris-Sud, Bâtiment 400, 91405 Orsay Cedex, France; CHRU de Tours, Université François Rabelais de Tours, UMR1282 ISP, F-37032 Tours, France; INRA, UMR1282 ISP, F-37380 Nouzilly, France.
Researchers developed a new tool, pG+off, for studying Streptococcus agalactiae, a major cause of neonatal infections. This tetracycline-inducible expression vector allows precise control over gene expression in the bacteria.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- Streptococcus agalactiae is a primary cause of neonatal infections.
- Genetic tools for studying Streptococcus agalactiae are limited, hindering research.
- Understanding Streptococcus agalactiae pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To develop a novel expression vector for Streptococcus agalactiae.
- To enable tightly-controllable gene expression in Streptococcus agalactiae.
- To facilitate genetic studies of Streptococcus agalactiae.
Main Methods:
- Development of pG+off, an expression vector.
- Incorporation of a tetracycline-inducible promoter.
- Validation using a reporter gene assay in Streptococcus agalactiae.
Main Results:
- The pG+off vector provides tightly-controllable gene expression.
- Demonstrated effective repression of gene expression under non-induced conditions.
- Confirmed functionality of the tetracycline-inducible promoter.
Conclusions:
- pG+off is a valuable new genetic tool for Streptococcus agalactiae research.
- The vector enables precise manipulation of gene expression.
- Facilitates further investigation into Streptococcus agalactiae biology and pathogenicity.
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