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Mutation in the Transcriptional Regulator PhoP Contributes to Avirulence of Mycobacterium tuberculosis H37Ra Strain

MPG-Autoren

Lee,  Jong Seok
Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50394

Krause,  Roland
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

Schreiber,  Jörg
Max Planck Society;

Mollenkopf,  Hans-Joachim
Max Planck Society;

Kowall,  Jane
Max Planck Society;

Stein,  Robert
Max Planck Society;

Patron,  Juan Pablo
Max Planck Society;

Jorg,  Sabine
Max Planck Society;

Kaufmann,  Stefan H.E.
Max Planck Society;

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Zitation

Lee, J. S., Krause, R., Schreiber, J., Mollenkopf, H.-J., Kowall, J., Stein, R., et al. (2008). Mutation in the Transcriptional Regulator PhoP Contributes to Avirulence of Mycobacterium tuberculosis H37Ra Strain. Cell Host & Microbe, 3(2), 97-103. doi:10.1016/j.chom.2008.01.002.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-8060-4
Zusammenfassung
Attenuated strains of mycobacteria can be exploited to determine genes essential for their pathogenesis and persistence. To this goal, we sequenced the genome of H37Ra, an attenuated variant of Mycobacterium tuberculosis H37Rv strain. Comparison with H37Rv revealed three unique coding region polymorphisms. One polymorphism was located in the DNA-binding domain of the transcriptional regulator PhoP, causing the protein's diminished DNA-binding capacity. Temporal gene expression profiles showed that several genes with reduced expression in H37Ra were also repressed in an H37Rv phoP knockout strain. At later time points, genes of the dormancy regulon, typically expressed in a state of nonreplicating persistence, were upregulated in H37Ra. Complementation of H37Ra with H37Rv phoP partially restored its persistence in a murine macrophage infection model. Our approach demonstrates the feasibility of identifying minute but distinct differences between isogenic strains and illustrates the consequences of single point mutations on the survival stratagem of M. tuberculosis.