NOTES The CorA Mg2 Channel Is Required for the Virulence of

CorA is the primary Mg2 channel in Salmonella enterica serovar Typhimurium. A corA mutant is attenuated in mice and defective for invasion of and replication within epithelial cells. Microarray studies show that several virulence effectors are repressed in a corA mutant strain, which ultimately manifests itself as a decrease in virulence. Salmonella enterica serovar Typhimurium causes infections that usually appear as a gastrointestinal ailment in more than 1.4 million Americans per year (50). Infection begins with oral consumption of live bacteria in contaminated food. In the small intestine, the bacteria are actively taken up by M cells of the Peyer’s patches and/or mononuclear phagocytes. A type three secretion system (TTSS) carried on Salmonella pathoge-nicity island 1 (SPI-1) delivers effector proteins to the M cell to aid in invasion (8, 14). Survival within the macrophage phago-some requires another TTSS encoded on SPI-2 (16, 28, 37). Thus, S. enterica serovar Typhimurium’s environment fluctu-ates markedly during its pathogenic life cycle and requires the coordination of expression of a multitude of virulence effectors and housekeeping genes. These gene products form dynamic signaling networks that interact to control the infection pro-cess. We asked if intracellular Mg2 of the bacterium is involved in virulence. To obtain Mg2, S. enterica serovar Typhimurium has three Mg2 transport systems. CorA, the primary or “housekeeping ” Mg2 channel, is constitutively expressed, while the MgtA and MgtB transporters are only expressed in response to activation by the PhoP/PhoQ two-component sys