The serine/threonine protein kinase PknI controls the growth of Mycobacterium tuberculosis upon infection

Radha Gopalaswamy, Sujatha Narayanan, Bing Chen, William R. Jacobs, Yossef Av-Gay

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

The protein kinase PknI is one of 11 functional serine/threonine protein kinases in Mycobacterium tuberculosis. Specialized transduction was performed to create a null mutant in the pknI gene. The resulting mutant was used to determine the role of PknI in M. tuberculosis growth and infectivity. The pknI mutant grows better under acidic pH and limited oxygen availability. We observed a modest increased growth of pknI mutant within macrophages during an in vitro infection and a hypervirulence phenotype in severe combined immunodeficiency mice. The internal signals used to activate PknI are most likely the host-associated signals such as low pH associated with limited oxygen availability. Thus, we have shown that PknI plays a role in sensing the host macrophage's environment and translating it to slow the growth of M. tuberculosis within the infected host.

Original languageEnglish (US)
Pages (from-to)23-29
Number of pages7
JournalFEMS Microbiology Letters
Volume295
Issue number1
DOIs
StatePublished - Jun 2009

Keywords

  • Infection
  • Macrophage
  • PknI
  • STPKs
  • Tuberculosis

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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