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The severity of symptoms elicited by the widespread human pathogen  Helicobacter pylori  is strongly influenced by the genetic diversity of the infecting strain. Among the most important pathogen factors that carry an increased risk for gastric cancer are specific genotypes of the  cag  pathogenicity island ( cag -PAI), encoding a type IV secretion system (T4SS) responsible for the translocation of the CagA effector oncoprotein. To date, little is known about the regulatory events important for the expression of a functional  cag -T4SS. Here we demonstrate that the  cag -PAI cistrons are subjected to a complex network of direct and indirect transcriptional regulations. We show that promoters of  cag  operons encoding structural T4SS components display homogeneous transcript levels, while promoters of  cag  operons encoding accessory factors vary considerably in their basal transcription levels and responses. Most  cag  promoters are transcriptionally responsive to growth-phase, pH and other stress-factors, although in many cases in a pleiotropic fashion. Interestingly, transcription from the P cagζ  promoter controlling the expression of transglycolase and T4SS stabilizing factors, is triggered by co-culture with a gastric cell line, providing an explanation for the increased formation of the secretion system observed upon bacterial contact with host cells. Finally, we demonstrate that the highly transcribed  cagA  oncogene is repressed by iron limitation through a direct  apo -Fur regulation mechanism. Together the results shed light on regulatory aspects of the  cag -PAI, which may be involved in relevant molecular and etiological aspects of  H. pylori  pathogenesis.

In Depth Analysis of the Helicobacter pylori cag Pathogenicity Island Transcriptional Responses