Bacterial chromatin remodeling associated with transcription-induced domains at pathogenicity Islands.
Salmonella Pathogenicity Islands (SPIs) are horizontally acquired genetic elements integrated in the chromosome of Salmonella species, which allow them to infect and survive within their hosts. The nucleoid associated protein H-NS silences SPI gene transcription and this repression is counter-silenced at precise stages of the Salmonella infectious cycle. Bistable expression of the Type Three Secretion System 1 encoded in SPI-1 is a key step in the invasion of epithelial cells by Salmonella. In bacteria, transcriptionally active units form chromatin domains with specific dynamics and subcellular localization.  How chromatin domains are formed in physiological conditions remains poorly characterized. By applying a functional genomics approach to phenotypically similar Salmonella populations, we studied the remodeling of SPI-1 chromatin upon H-NS counter silencing. Our results show that although H-NS significantly reduces pervasive transcription, high H-NS occupancy co-exists with a low spurious transcriptional activity and low RNA polymerase occupancy at silent SPIs. When SPI-1 is expressed, we observe a remodeling of SPI-1 chromatin into domains that is dependent on the HilD transcriptional regulator. We uncovered the transcriptional signature of Salmonella cells expressing SPI-1 and determined that SPI-1 chromatin domains are associated with a variable distribution of H-NS occupancy and localized close to the nucleoid periphery. Our findings support a model in which the transcriptional activation of SPI-1 genes drives the chromatin remodeling and subcellular re-localization of this pathogenicity island. Overall design: Chromomosome conformation capture, RNA-seq and ChIP-seq of Salmonella enterica serovar Thyphimurium SL1344 WT and hilE mutant.