Journal
FEMS MICROBIOLOGY LETTERS
Volume 287, Issue 2, Pages 181-184Publisher
OXFORD UNIV PRESS
DOI: 10.1111/j.1574-6968.2008.01309.x
Keywords
protein tyrosine phosphatase; PtpA; in vivo phenotype; growth rate
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Funding
- National Institutes of Health
- American Lung Association, California
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Mycobacterium tuberculosis (Mtb) alters the host response to infection by secreting protein factors. Mtb produces two secreted protein tyrosine phosphatases, PtpA and PtpB, which are thought to interfere with host signaling. Deletion of ptpA or ptpB attenuates bacterial growth in activated macrophages. To address the in vivo function of PtpA, we generated a genetic deletion mutant, Delta ptpA. The mutant was not defective when grown in vitro, consistent with the presumed role of PtpA in the host. The ptpA mutant, however, also showed no growth defect in a mouse infection model. The absence of a growth defect in mice suggests that the requirement for PtpA differs in mouse and human infections, and that mice are not a suitable infection model for the study of PtpA.
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