Campylobacter jejuni is a leading bacterial cause of acute gastroenteritis in the United States; campylobacteriosis is also associated with the development of post-infection sequelae such as Guillain-Barré Syndrome.  C. jejuni inhabits multiple hosts and environmental niches, which necessitates that it regulate protein expression in response to numerous external signals.  Because C. jejuni lacks many of the transcriptional regulatory proteins found in other enteric pathogens, my lab studies the post-transcriptional regulator CsrA.  In other bacteria, CsrA-mediated regulation involves binding of CsrA to mRNAs of target genes, resulting in diverse outcomes on protein expression.  CsrA activity is controlled by competitive binding to one or more small RNAs (sRNAs) that titrate CsrA activity, resulting in decreased CsrA binding to target mRNAs. The sRNAs are in turn regulated by environmental conditions, allowing sRNA antagonism of CsrA to be modulated.  In C. jejuni, mutation of csrA results in changes in protein expression and changes in this organism’s virulence properties.