SPI-1 virulence gene expression modulates motility ofSalmonellaTyphimurium in a proton motive force- and adhesins-dependent manner

Abstract

AbstractBoth the bacterial flagellum and the evolutionary related injectisome encoded on theSalmonellapathogenicity island 1 (SPI-1) play crucial roles during the infection cycle ofSalmonellaspecies. The interplay of both is highlighted by the complex cross-regulation that includes transcriptional control of the flagellar master regulatory operonflhDCby HilD, the master regulator of SPI-1 gene expression. Contrary to the HilD-dependent activation of flagellar gene expression, we report here that activation of HilD resulted in a dramatic loss of motility, which was dependent on the presence of SPI-1. Single cell analyses revealed that HilD-activation results in a SPI-1-dependent induction of the stringent response and a pronounced decrease of proton motive force (PMF), while flagellation was not affected. We further found that activation of HilD enhanced the adhesion ofSalmonellato epithelial cells. A transcriptome analysis revealed a concomitant upregulation of several adhesin systems, which when overproduced, phenocopied the HilD-induced motility defect. We propose that a combination of SPI-1-dependent depletion of the PMF and upregulation of adhesins upon HilD-activation allows flagellatedSalmonellato rapidly modulate their motility during infection, thereby enabling efficient adhesion to host cells and delivery of effector proteins.