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The enteropathogen  Yersinia pseudotuberculosis  and the related plague agent  Y .  pestis  require the Ysc type III secretion system (T3SS) to subvert phagocyte defense mechanisms and cause disease. Yet type III secretion (T3S) in  Yersinia  induces growth arrest and innate immune recognition, necessitating tight regulation of the T3SS. Here we show that  Y .  pseudotuberculosis  T3SS expression is kept low under anaerobic, iron-rich conditions, such as those found in the intestinal lumen where the  Yersinia  T3SS is not required for growth. In contrast, the  Yersinia  T3SS is expressed under aerobic or anaerobic, iron-poor conditions, such as those encountered by  Yersinia  once they cross the epithelial barrier and encounter phagocytic cells. We further show that the [2Fe-2S] containing transcription factor, IscR, mediates this oxygen and iron regulation of the T3SS by controlling transcription of the T3SS master regulator LcrF. IscR binds directly to the  lcrF  promoter and, importantly, a mutation that prevents this binding leads to decreased disseminated infection of  Y .  pseudotuberculosis  but does not perturb intestinal colonization. Similar to  E .  coli ,  Y .  pseudotuberculosis  uses the Fe-S cluster occupancy of IscR as a readout of oxygen and iron conditions that impact cellular Fe-S cluster homeostasis. We propose that  Y .  pseudotuberculosis  has coopted this system to sense entry into deeper tissues and induce T3S where it is required for virulence. The IscR binding site in the  lcrF  promoter is completely conserved between  Y .  pseudotuberculosis  and  Y .  pestis . Deletion of  iscR  in  Y .  pestis  leads to drastic disruption of T3S, suggesting that IscR control of the T3SS evolved before  Y .  pestis  split from  Y .  pseudotuberculosis .

Iron availability and oxygen tension regulate the Yersinia Ysc type III secretion system to enable disseminated infection