RtsA can directly induce the hilA expression independent of HilD .
RtsA can directly induce the hilA expression independent of HilC .
In the present study , the expression from lac fusion was retained after disruption in Fig. 2A in cells , suggesting the contribution of RtsA on the expression from the hilA promoter in these mutants .
In the present study , the expression from the hilA was retained after disruption in Fig. 2A in cells , suggesting the contribution of RtsA on the expression from the hilA promoter in these mutants .
RtsA increases invasion gene expression by increasing transcription of hilA .
These data suggest that RtsA may activate hilA expression in response to a set of signals .
Like HilD , RtsA activates expression of SPI1 genes by binding upstream of the master regulatory gene hilA to induce its expression .
Like HilC , RtsA activates expression of SPI1 genes by binding upstream of the master regulatory gene hilA to induce its expression .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of rtsA We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of rtsA We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of hilD We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of hilD We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of hilC We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , RtsA can independently induce expression of hilC We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of rtsA We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of rtsA We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of hilD We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of hilD We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of hilC We have shown that RtsA , like HilD , induces expression of hilA by binding to the HilA promoter region .
Thus these regulators form a self-reinforcing feed forward regulatory loop and increased expression or activity of one regulator leads to an increase in expression of the other regulators Results HilC , HilD can independently induce expression of hilC We have shown that RtsA , like HilC , induces expression of hilA by binding to the HilA promoter region .
We wanted to determine if RtsA could induce expression of hilA in the absence of the other regulators .
The data in Fig. 2 demonstrate that RtsA are able to induce expression of hilA in the absence of the other regulators .
Production of HilC induced expression of hilA ~ 120-fold , while RtsA induced expression of hilA 30-to 40-fold , similar to previously reported values .
We show that RtsA can each independently activate expression of the hilA genes .
However , RtsA normally act in concert to activate hilA .
RtsA can activate expression of hilA .
The mechanism by which RtsA activate expression of hilA
That means that at least hilA are induced by RtsA proteins .
Under high-osmolarity conditions , RtsA activate SPI1 genes indirectly through hilA .
Under high-osmolarity conditions , RtsA activate SPI1 genes directly through hilA .
RtsA are each capable of activating hilA transcription .
Earlier work on mathematical modeling of regulation of expression of hilA by RtsA was based on feed-forward architecture , considering HilD to be the primary activator of the feed-forward loop .
RtsA are central activators of hilA expression ( Ellermeier et al. , 2005 ; 2001 ; Schechter et al. , Abbreviations : Cy , Cyanine ; SSC , saline sodium citrate ; SPI1 , Salmonella pathogenicity island 1 ; S. Typhimurium , Salmonella enterica serovar Typhimurium ; TTSS , type III secretion system .
RtsA are central activators of hilA expression ( Ellermeier et al. , 2005 ; Lee ; Schechter et al. , Abbreviations : Cy , Cyanine ; SSC , saline sodium citrate ; SPI1 , Salmonella pathogenicity island 1 ; S. Typhimurium , Salmonella enterica serovar Typhimurium ; TTSS , type III secretion system .
RtsA are central activators of hilA expression ( Ellermeier et al. , 2005 ; Lucas ; Schechter et al. , Abbreviations : Cy , Cyanine ; SSC , saline sodium citrate ; SPI1 , Salmonella pathogenicity island 1 ; S. Typhimurium , Salmonella enterica serovar Typhimurium ; TTSS , type III secretion system .
hilA expression is induced by three transcriptional activators , RtsA .
Inducible expression RtsA protein was sufficient to activate hilA following growth at 42 °C .
Transcription of the hilA gene is also stimulated by RtsA .