Abstract
The ability to sense the temperature of surrounding environments is a prerequisite for many bacterial pathogens to adjust their virulence program to establish an infection. Pathogenic Yersinia species use intrinsic thermosensing protein domains and mRNA secondary structures of crucial virulence regulators to activate essential colonization factors during the early infection stage and induce antiphagocytic strategies to prevent attacks of the innate host immune system during the ongoing infection.
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