Protein tyrosine phosphatase PtpA is not required for Mycobacterium tuberculosis growth in mice

被引:32
|
作者
Grundner, Christoph [1 ]
Cox, Jeffery S. [2 ]
Alber, Tom [1 ]
机构
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
基金
美国国家卫生研究院;
关键词
protein tyrosine phosphatase; PtpA; in vivo phenotype; growth rate;
D O I
10.1111/j.1574-6968.2008.01309.x
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:181 / 184
页数:4
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