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J. Biol. Chem., Vol. 279, Issue 22, 23082-23087, May 28, 2004
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Two Sensor Kinases Contribute to the Hypoxic Response of Mycobacterium tuberculosis*
¶¶
From the
Department of Pathobiology, School of Public Health and Community Medicine, ¶Department of Biochemistry, ||Biomolecular Structure Center, **Biomolecular Structure and Design Graduate Program, and Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195
Current estimates indicate that nearly a third of the world's population is latently infected with Mycobacterium tuberculosis. Reduced oxygen tension and nitric oxide exposure are two conditions encountered by bacilli in vivo that may promote latency. In vitro exposure to hypoxia or nitric oxide results in bacterial stasis with concomitant induction of a 47-gene regulon controlled by the transcription factor DosR. In this report we demonstrate that both the dosS gene adjacent to dosR and another gene, dosT (Rv2027c), encode sensor kinases, each of which can autophosphorylate at a conserved histidine and then transfer phosphate to an aspartate residue of DosR. Mutant bacteria lacking both sensors are unable to activate expression of DosR-regulated genes. These data indicate that DosR/DosS/DosT comprise a two-component signaling system that is required for the M. tuberculosis genetic response to hypoxia and nitric oxide, two conditions that produce reversible growth arrest in vitro and may contribute to latency in vivo.
Received for publication, February 4, 2004 , and in revised form, March 12, 2004.
* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Supported by National Institutes of Health Training Grant AI07509 awarded to the University of Washington Pathobiology Department.
Supported by National Institutes of Health Grant CA65656.
¶¶ Supported by National Institutes of Health Grant AI47744. To whom correspondence should be addressed. Tel.: 206-221-5381; Fax: 206-543-3873; E-mail: dsherman{at}u.washington.edu.
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