JAC Advance Access published online on April 29, 2004
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh215
© 2004 by The British Society for Antimicrobial Chemotherapy
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1 Tuberculosis Research
Lead Programme, Medical Research Council, Pretoria;
* To whom correspondence should be addressed. E-mail: randerso{at}medic.up.ac.za.
We have used a phospholipase C (PLC)-deletion mutant
(plcABC) of the H37Rv strain of Mycobacterium tuberculosis (MTB),
as well as a plcA-insertion mutant of Mycobacterium
smegmatis, to investigate the possible involvement of PLCs
in clofazimine-mediated inhibition of mycobacterial K+ transport
and growth. Inactivation of the PLCs of MTB and insertion of the plcA gene into M. smegmatis resulted
in a substantial reduction and increase in hydrolysis of phosphatidylcholine
(PC), respectively. However, both the mutant and wild-type strains
of MTB and M. smegmatis were equally sensitive
to the inhibitory effects of clofazimine on K+ uptake
and growth. These observations demonstrate that the PLCs of MTB
are not involved in the antimicrobial activity of clofazimine.
Accepted February 27, 2004
Original article
Antimicrobial activity of clofazimine is not dependent
on mycobacterial C-type phospholipases
2 Medical Research Council Unit
for Inflammation and Immunity, Department of Immunology, Faculty
of Health Sciences, University of Pretoria,
PO Box 2034, Pretoria 0001, South Africa
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