Rv2190c, an NlpC/P60 Family Protein, Is Required for Full Virulence of Mycobacterium tuberculosis

University of Padova, Italy
PLoS ONE (Impact Factor: 3.23). 08/2012; 7(8):e43429. DOI: 10.1371/journal.pone.0043429
Source: PubMed


Mycobacterium tuberculosis, the etiologic agent of tuberculosis (TB) possesses at least five genes predicted to encode proteins with NlpC/P60 hydrolase domains, including the relatively uncharacterized Rv2190c. As NlpC/P60 domain-containing proteins are associated with diverse roles in bacterial physiology, our objective was to characterize Rv2190c in M. tuberculosis growth and virulence. Our data indicate that lack of Rv2190c is associated with impaired growth, both in vitro and during an in vivo mouse model of TB. These growth defects are associated with altered colony morphology and phthiocerol dimycocerosate levels, indicating that Rv2190c is involved in cell wall maintenance and composition. In addition, we have demonstrated that Rv2190c is expressed during active growth phase and that its protein product is immunogenic during infection. Our findings have significant implications, both for better understanding the role of Rv2190c in M. tuberculosis biology and also for translational developments.

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Available from: Haidan Guo
    • "Our data suggests that Rv0024 may be responsible for alteration in mycobacterial cell wall lipids associated with cell wall assembly and bacterial replication. Previous studies has shown that deletion of Rv2190, another member of the same hydrolase family in Mtb, caused displacement of Phthiocerol dimycocerosate in the cell wall and also affected septation process during cell division [22]. However, we did not see any difference in the septum formation in MsmRv0024 and pSMT3 strains. "
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    • "Rv2190c encodes another NlpC/P60-type PG hydrolase in mycobacteria. Deletion of this gene in M. tuberculosis results in altered colony morphology, attenuated growth in vitro, defective PDIM production and reduced colonisation of mouse lungs in the murine model of TB infection [64]. Consistent with this, homologues of Rv2190c are found in all pathogenic mycobacteria, Table  1, with notable genetic expansion in some environmental species. "
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