Although it has been proposed that SirA directly controls expression of both hilC , it was also determined that HilC was not required for SirA to control hilA expression .
Our model suggests that SirA could control expression of hilC by regulating the expression of a single regulator .
Our model suggests that SirA could control expression of hilC by either independently activating each gene .
This suggests that SirA regulates expression of hilC via HilD .
This genetic analysis is apparently inconsistent with previous gel shift data suggesting that SirA binds both the hilC .
Once phosphorylated , SirA directly binds the hilC promoters .
SirA controls these genes by directly binding hilC regulatory genes .
Conversely , previously published gel-shift data suggested that SirA is able to bind to the promoters of hilC .
Whereas SirA might bind to the hilC promoters during in-vitro gel-shift experiments , genetic data shows that SirA is incapable of directly activating these promoters ; SirA binding to DNA in-vitro does not represent activation .
To check if both regulators are important , the regulation of hilC gene expression by SirA is considered to check the possibility of one of the regulators being important , this dependency is taken as an OR gate .
To check if both regulators are important , the regulation of hilC gene expression by SirA is considered to function as gate , this dependency is taken as an OR gate .
To check if both regulators are important , the regulation of hilC gene expression by SirA is considered to function as an , this dependency is taken as an OR gate .
SirA , directly regulates the hilC genes at the top of the invasion cascade .