Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 38, Pages 14591-14596Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0801205105
Keywords
H-NS; OmpR; microbial pathogenesis; transcriptional regulation; salmonella
Categories
Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACYT) [42918Q, 169380]
- Howard Hughes Medical Institute [75301-565101]
- Direccion General de Asuntos del Personal Academico (DGAPA) [IN227306-3]
- Intramural Research Program of the National Institute of Allergy and Infectious Diseases
- National Institutes of Health
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The acquisition of new genetic traits by horizontal gene transfer and their incorporation into preexisting regulatory networks have been essential events in the evolution of bacterial pathogens. An example of successful assimilation of virulence traits is Salmonella enterica, which acquired, at distinct evolutionary times, Salmonella pathogenicity island 1 (SPI-1), required for efficient invasion of the intestinal epithelium and intestinal disease, and SPI-2, essential for Salmonella replication and survival within macrophages and the progression of a systemic infection. A positive regulatory cascade mainly composed of HilD, HilA, and InvF, encoded in SPI-1, controls the expression of SPI-1 genes, whereas the two-component regulatory system SsrA/B, encoded in SPI-2, controls expression of SPI-2 genes. In this study, we report a previously undescribed transcriptional cross-talk between SPI-1 and SPI-2, where the SPI-1-encoded regulator Hill) is essential for the activation of both the SPI-1 and SPI-2 regulons but at different times during the stationary phase of growth in Luria-Bertani medium. Our data indicate that HilD counteracts the H-NS-mediated repression exerted on the OmpR-dependent activation of the ssrAB operon by specifically interacting with its regulatory region. In contrast, HilD is not required for SPI-2 regulon expression under the in vitro growth conditions that are thought to resemble the intracellular environment. Our results suggest that two independent SPI-2 activation pathways evolved to take advantage of the SPI-2-encoded information at different niches and, in consequence, in response to different growth conditions.
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