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Background  A previous study identified a  Yersinia enterocolitica  transposon mutant, GY448, that was unable to export the flagellar type three secretion system (T3SS)-dependent phospholipase, YplA. This strain was also deficient for motility and unable to form colonies on Lauria-Bertani agar medium. Preliminary analysis suggested it carried a mutation in  csrA . CsrA in  Escherichia coli  is an RNA-binding protein that is involved in specific post-transcriptional regulation of a myriad of physiological activities. This study investigated how CsrA affects expression of the flagellar regulatory cascade that controls YplA export and motility. It also explored the effect of  csrA  mutation on  Y. enterocolitica  in response to conditions that cue physiological changes important for growth in environments found both in nature and the laboratory.    Results  The precise location of the transposon insertion in GMY448 was mapped within  csrA . Genetic complementation restored disruptions in motility and the YplA export phenotype (Yex), which confirmed this mutation disrupted CsrA function. Mutation of  csrA  affected expression of  yplA  and flagellar genes involved in flagellar T3SS dependent export and motility by altering expression of the master regulators  flhDC . Mutation of  csrA  also resulted in increased sensitivity of  Y. enterocolitica  to various osmolytes, temperatures and antibiotics.    Conclusions  The results of this study reveal unique aspects of how CsrA functions in  Y. enterocolitica  to control its physiology. This provides perspective on how the Csr system is susceptible to adaptation to particular environments and bacterial lifestyles.

CsrA impacts survival of Yersinia enterocolitica by affecting a myriad of physiological activities