Deletion of the rel gene in Mycobacterium smegmatis reduces its stationary phase survival without altering the cell-surface associated properties

Dormant or latent physiology of the mycobacterial species is a subject of current investigation in order to understand the long-term persistence of these organisms inside the host. It is argued that the carbonstarved mycobacteria may serve as a good model for the dormant bacilli. The relA/spoT gene...

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Bibliographic Details
Published inCurrent science (Bangalore) Vol. 86; no. 1; pp. 149 - 153
Main Authors Mathew, Renjith, Ojha, Anil Kr, Karande, Anjali A., Chatterji, Dipankar
Format Journal Article
LanguageEnglish
Published Current Science Association 10.01.2004
Subjects
Bacteria
Cell lines
Cultured cells
DNA
Inoculum
Macrophages
Mycobacterium smegmatis
Mycobacterium tuberculosis
SPECIAL SECTION: TUBERCULOSIS
Starvation
Steepest descent method
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ISSN0011-3891

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Summary:Dormant or latent physiology of the mycobacterial species is a subject of current investigation in order to understand the long-term persistence of these organisms inside the host. It is argued that the carbonstarved mycobacteria may serve as a good model for the dormant bacilli. The relA/spoT gene is upregulated during carbon starvation in Mycobacterium tuberculosis and the deletion of the gene resulted in reduction of long-term persistence in M. tuberculosis. Overexpression of the gene in M. smegmatis changes the colony morphology of the bacteria. Here we show that knock-out of the relA/spoT gene compromises stationary-phase survival of M. smegmatis. However, the ΔrelA/spoT bacteria show similar profile of glycopeptidolipids as the wild-type bacteria under carbon starvation. We have seen here that M. smegmatis, a nonpathogenic species, upon carbon starvation exhibits reduced association with murine macrophage cell line RAW 264.7 in comparison to M. smegmatis grown in carbon-enriched medium. But the clearance of the bacteria from macrophages takes place in the same window of time in both conditions.
ISSN:0011-3891