Gene targets included : 16S rDNA ( Lin and Tsen 1996 ) , a Salmonella pathogenicity island I virulence gene ( hilA ) ( Guo et al. 2000 ) , Salmonella enterotoxin gene ( stn ) ( Makino et al. 1999 ) , invA gene ( Ferretti et al. 2001 ) , Fur-regulated gene ( iroB ) ( Bäumler et al. 1997 ) , histidine transport operon ( Cohen et al. 1993 ) , the junction between sipB and sipC virulence genes ( sipB-sipC ) ( Carlson et al. 1999 ) , a Salmon-ella-specific repetitive DNA fragment ( Jitrapakdee et al. 1995 ) , and a multiplex targeting invA gene and spvC gene of the virulence plasmid ( invA/spvC ) ( Chiu and Ou 1996 ) .
In this work , we demonstrated that Fur regulates expression of hilA via control of HilD .
that Fur plays a major role in this metal regulation of hilA and therefore SPI1 expression
Taken together , these data indicate that Fur acts as a positive regulator of hilA expression .
Fur regulates expression of hilA by working through HilD .
Having established that Fur controls hilA expression , we wanted to see how Fur fits into the feed forward loop model of SPI1 regulation that we previously defined .
Figure 3 shows that Fur regulation of hilA was abrogated in any background ; in all hilD strains there was no significant difference in hilA expression between the fur strains .
Figure 3 shows that Fur regulation of hilA was abrogated in any background ; in all hilD strains there was no significant difference in hilA expression between the fur strains .
As expected , based on our model , deletion of rtsA affected the overall expression of hilA but di not prevent Fur regulation of hilA .
As expected , based on our model , deletion of hilC affected the overall expression of hilA but di not prevent Fur regulation of hilA .
To further test the requirement for HilD for Fur-mediated regulation of hilA , we examined the effects of Fur overexpression in strains .
This provides clear genetic evidence that HilD is absolutely required for Fur regulation of hilA .
Given that HilD is required for Fur regulation of hilA , it seemed possible that Fur regulates hilD expression in some manner .
Fur regulates expression of hilA via HilD .
However , the data suggest that Hfq plays no role in the Fur regulation of hilA , again differentiating sodB regulation .
However , the data suggest that Hfq plays no role in the Fur regulation of hilA , again differentiating SPI1 regulation .
However , the data suggest that Hfq plays little role in the Fur regulation of hilA , again differentiating sodB regulation .
However , the data suggest that Hfq plays little role in the Fur regulation of hilA , again differentiating SPI1 regulation .
Fur does not regulate hilA expression by controlling HilE .
Fur regulation of hilA are mechanistically different .
Either way , Fur regulates hilA by posttranslationally affecting the HilD protein .
Also , while deletion of rtsA affected the fold effect of fur , it did not prevent Fur regulation of hilA .
Also , while deletion of rtsA decreased the expression of hilA , it did not prevent Fur regulation of hilA .
Also , while deletion of hilC affected the fold effect of fur , it did not prevent Fur regulation of hilA .
Also , while deletion of hilC decreased the expression of hilA , it did not prevent Fur regulation of hilA .