Both hypotheses need to be tested , but we already know that expression of sdiA from a plasmid increases the expression of SdiA-regulated genes in the absence of signal ( 1 , 22 ) .
Given that the Salmo-nella promoters are confirmed to respond to chromosomal sdiA and AHL , whereas the ftsQP2 promoter is not , we suspect that the binding of SdiA to the ftsQP2 promoter may not be physiologically relevant .
Despite the regulation of putative virulence genes by SdiA , we have previously reported that an sdiA mutant of S. Typhimurium is not attenuated in cow models of infection .
Despite the regulation of putative virulence genes by SdiA , we have previously reported that an sdiA mutant of S. Typhimurium is not attenuated in chicken .
Despite the regulation of putative virulence genes by SdiA , we have previously reported that an sdiA mutant of S. Typhimurium is not attenuated in mouse .
Despite the regulation of putative virulence genes by SdiA , a sdiA mutant of S. enterica sv .
Therefore , binding of plant compounds to SdiA can not explain the lack of sdiA expression in planta .
It seems that SdiA needs the binding of AHLs for proper protein folding before interacting with DNA although some studies suggested that the overexpression of sdiA could be sufficient to activate it -LRB- without AHLs -RRB- .
In mice , infection with a sdiA mutant resulted in increased bacterial loads in the livers of infected mice indicating that SdiA may be a negative regulator of virulence .
In mice , infection with a sdiA mutant resulted in increased fecal shedding in the livers of infected mice indicating that SdiA may be a negative regulator of virulence .
To test this hypothesis , we determined that S. typhimurium encodes SdiA regulated by sdiA .