Open AccessProtein tyrosine phosphatase PtpA is not required for Mycobacterium tuberculosis growth in mice
Author(s) -
Grundner Christoph,
Cox Jeffery S.,
Alber Tom
Publication year - 2008
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2008.01309.x
Subject(s) - mutant , protein tyrosine phosphatase , mycobacterium tuberculosis , biology , phosphatase , in vivo , in vitro , tyrosine , microbiology and biotechnology , tuberculosis , phosphorylation , biochemistry , gene , genetics , medicine , pathology
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, Δ 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.