Abstract
Salmonella enterica pathogenicity island 1 (SPI-1) is a gene cluster that encodes a type III secretion system and effectors involved in epithelial cell invasion. SPI-1 undergoes bistable expression, with concomitant formation of SPI-1ON and SPI-1OFF lineages. This study describes single cell analysis of SP1-1 bistability and epithelial cell invasion, and reports the unsuspected observation that optimal invasion of epithelial cells requires the presence of both SPI-1ON and SPI-1OFF subpopulations. The contribution of SPI-1OFF cells to optimal invasion may rely on their ability to invade epithelial cells if a SPI-1ON subpopulation is present. In fact, Salmonella SPI-1 mutants are also able to invade epithelial cells in the presence of SPI-1ONSalmonellae, a phenomenon described in the 1990’s by Galán and co-workers. Invasion by SPI-1OFF cells does not seem to involve a diffusible factor. A small number of SPI-1ON cells is sufficient to endow the bacterial population with invasion capacity, a feature that may permit host colonization regardless of the bottlenecks encountered by Salmonella populations inside animals.
Highlights
SP1-1 bistability and epithelial cell invasion, and reports the unsuspected observation that optimal invasion of epithelial cells requires the presence of both SPI-1ON and SPI-1OFF subpopulations
Invasion of epithelial cells by S. enterica serovar Typhimurium requires the expression of genes encoded on pathogenicity island 1 (SPI-1)
To monitor expression of Salmonella enterica pathogenicity island 1 (SPI-1) at the single cell level, transcriptional green fluorescent protein (GFP) fusions were constructed downstream of three SPI-1 genes: sipB, which encodes an effector of SPI-1 ; prgH, encoding a component of the T3SS apparatus; and hilA, a regulatory gene that encodes a transcriptional activator of SPI-1 operons
Summary
SP1-1 bistability and epithelial cell invasion, and reports the unsuspected observation that optimal invasion of epithelial cells requires the presence of both SPI-1ON and SPI-1OFF subpopulations. Phase variation of the Salmonella enterica opvAB operon generates a bacterial subpopulation that is resistant to phages at the expense of virulence attenuation[14] Another example of tradeoff may be found in phase-variable glycosyltransferase (gtr) operons[15], whose products are crucial for intestinal persistence and faecal shedding of Salmonella but reduce invasion of both epithelial cells and macrophages[16]. In both examples, programmed reversion of the bistable states regenerates heterogeneity and sustains the tradeoff. SPI-1 is a ~40 kb gene cluster that encodes a type III secretion system (T3SS) and www.nature.com/scientificreports/
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
