NEW FINDINGS ON THE INTERACTION BETWEEN RCSB AND SLYA TO CONTROL Salmonella Typhimurium VIRULENCE

FLORENCIA BALLESTEROS; MONICA F. TORREZ-LAMBERTI; JUAN V. FARIZANO; MARÍA DE LAS MERCEDES PESCARETTI; MÓNICA A. DELGADO

CABA

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

SOCIEDADES DE BIOCIENCIAS

The Salmonella Typhimurium RcsCDB system regulates the synthesisof colanic acid and flagellum as well as the expression ofnumerous virulence genes. We previously demonstrated that thercsC11 mutant, which constitutively activates the RcsB regulator,attenuates Salmonella virulence in an animal model. In addition, thisattenuated phenotype could be also produced by deletion of the slyAgene. In this work we investigated if this antagonistic behavior isproduced by the modulation of the expression of both regulator-encodinggenes. We demonstrated that SlyA overproduction negativelyregulates rcsB transcription. A bioinformatic analysis allowedus to identify a putative SlyA binding site on each of both promoters,PrcsDB and PrcsB, which control rcsB levels. In addition, we determinedthat SlyA is able to recognize and bind to these predicted sites tomodulate the activity of both rcsB promoters. According to these results,SlyA represses rcsB transcription by direct binding to specificsites located on the rcsB promoters, thus accounting for the aboveantagonistic behavior. Moreover, we showed that the opposite effectbetween both regulators also physiologically affects the Salmonellamotility phenotype. In this sense, we observed that under SlyA overproductionthe PrcsB is repressed and consequently bacterial motility is increased. On the basis of these results, we suggest that duringinfection the different RcsB levels produced act as a switch betweenthe Salmonella virulent or attenuated form. Thereby, we proposethat higher concentrations of RcsB tilt the balance towards the attenuatedform, while absence or low concentrations resulting fromSlyA overproduction does it towards the virulent form.