Add repository structure and files

+---
+title: "Untagged word counter"
+output: html_notebook
+---
+Description: Counts the frequency of words mentioned in each untagged sentence without taking into consideration stop words. 
+
+```{r}
+library(dplyr)
+library(tidytext)
+library(tidyverse)
+```
+
+
+
+```{r}
+annotations <- read.csv("../results/annotationsExt_features.csv")
+
+# Keeping only sentences without organism recognition
+zero_annotations<- annotations %>%
+  filter(NumberOfOrganism == 0)
+
+# Spliting Sentences into one-token-per-row
+zero_tokens<- unnest_tokens(zero_annotations, output = "tokens", input ="Sentence",token ="words",format ="text")
+
+# Check words most frequently used without tidying stop words
+zero_tokens %>%
+  count(tokens) %>%
+  arrange(desc(n))
+
+# loading stop words english dictionary 
+data("stop_words")
+
+# Keeping all tokens that are not in stop words dictionary
+tidy_tokens<-zero_tokens %>%
+  anti_join(stop_words, by = c("tokens" ="word"))
+
+# Checking most frequent tidy tokens
+tidy_tokens %>%
+  count(tokens) %>%
+  arrange(desc(n))
+
+# Checking less frequent tidy tokens
+tidy_tokens %>%
+  count(tokens) %>%
+  arrange(n)
+```
+
+

+O moregulated ProP Protein f Salmonella E Serovar Typhimurium of mino s o nterica 1 
+strain TL4513 ( proP4 : : Tn10dCm DproBA47 DputPA573 proU1884 : : MudJ ) , using the linked melA : : Tn10 as the selected marker .\n"
+Strains TL4554-TL4559 and the isogenic proP strain TL4553
+generating strains TL4533-TL4535 , TL4544-TL4546 , and TL4560 
+yielding strains TL4627-TL4633 
+proline auxotrophs TL1673 and TL4500
+from TL4500 
+TL1901 
+and the M65R , S73F , L89R , and S284R mutants (oracioón 122)
+
+serovar Typhimurium
+S. enterica serotypes represented are Typhimurium ( ST ) , Enteritidis ( SE ) , Heidelberg ( SH ) , Infantis ( SI ) and Seftenberg ( SS ) .
+SCV , Salmonella-containing vacuole ; casp-1 , caspase-1 .
+Accumulation of-tubulin was detected around SCV containing replicating S. bongori ( pB6 ) but was not observed in HeLa cells infected with S. bongori .
+Growth phase-regulated induction of Salmonella-induced macrophage apoptosis correlates with transient expression of SPI-1 genes .
+These two are nontyphoid Salmonella ( NTS ) serovars that are capable of causing disease signs in a variety of animals , which contrasts with typhoid fever serovars that exclusively infect humans .
+Mid-logarithmic cultures of Salmonella serovar Typhi-murium SL1344 were produced and adapted for 2 h with 0.015 M lactic-acid in tryptone soy broth ( TSB ) ( Difco ) at pHo 5.8 as previously described ( 9 ) .
+Differences in the LPS of Salmonella ( S. ) enterica determine the many serovars in this genus ( Lüderitz et al. 1966 ) .
+A Salmonella serovar Typhimurium DT104 strain in which the dam gene was replaced ( strain RAK102 ) with the aminoglycoside phosphotransferase gene ( aph ) encoding kanamycin resistance was constructed by allelic exchange by using a previously described method , with minor modifications ( 8 ) .
+S. enterica subspecies I serotype Typhimurium NCTC 12023 ( S. enterica serotype Typhimurium ) was used as a wild-type strain .
+Salmonella consists of two species , bongori and enterica , and the latter can be further divided into subspecies ( I-VI ) .
+The six subspecies that define S. enterica ( enterica [ I ] , salamae [ II ] ) , arizonae [ IIIA ] , diarizonae [ IIIB ] , houtenae [ IV ] , and indica [ VI ] ) constitute in excess of 2500 recognized serovars .
+While subspecies Braenderup Agona ( 1 ) Hadar ( 1 ) Paratyphi B var .
+The remaining subspecies have been renamed under the S. enterica species as enterica ( I ) , salamae ( II ) , arizonae ( IIIa ) , diarizo-nae ( IIIb ) , houtenae ( IV ) , and indica ( VI ) , which are further divided into over 2,600 serovars based on their O ( oligosaccharide ) and H ( flagellar ) antigens ( 2 ) .
+Subspecies names are symbolized as follows : S. enterica subspecies enterica ( I ) , S. enterica subspecies salamae ( II ) , S. enterica subspecies arizonae ( IIIa ) , S. enterica subspecies diarizonae ( IIIb ) , and S. enterica subspecies houtenae ( IV ) .
+Salmonella serovar Typhi Ty21a was grown in LB broth or tryptic soy broth or on tryptic soy agar supplemented with 0.01 % galactose ( Sigma-Aldrich , St. Louis , MO ) .
+All S. Typhi strains are derived from the z66-positive wild-type strain GIFU10007 [ 12 ] .
+Unlike `` classical '' non-typhoidal Salmonella ( NTS ) , gastroenteritis is often absent during ST313 infections and isolates are most commonly recovered from blood , rather than from stool .
+Murine J774A .1 macrophages were infected with S. enterica serovar Typhimurium UK1 WT , DraoN and complemented strains and the numbers of viable intracellular bacteria were determined at 4 h and 20 h after infection .
+
+
+
+
+
+
+
+salmonella
+salmonellae
+Salmonellae
+Salmonellaenterica
+typhi
+enterica
+bongori
+serovar
+enteritidis
+typhimurium
+Typhimurium
+serovars
+typhoid 
+S. Typhi
+S. flexneri
+S. enterica
+sl1344 
+Salmonella spp.
+monella
+Sal-monella
+NTS
+non-typhoidal
+nontyphoidal
+Typhi-murium
+typhi-murium
+SL1344
+Salmonellas
+Salmonella-infected
+Salmonella-specific 
+Salmonella-mediated
+DT104
+paratyphi
+Paratyphi
+Ty21a
+DT104
+GIFU10007
+sl7207
+sl3261
+typhimu
+typhoidal
+G785
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+The dps promoter is activated by IHF S in stationary-phase .
+M , G. 1994 The dps promoter is activated by IHF and s in stationary-phase .
+The dps promoter is activated by IHF S in stationary-phase .
+The dps promoter is activated by IHF in stationary-phase .
+The dps promoter is activated by IHF S in stationary-phase .
+The dps promoter is activated by IHF in stationary-phase .
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+The dps promoter is activated by IHF S in stationary-phase .
+M , G. 1994 The dps promoter is activated by IHF and s in stationary-phase .
+The dps promoter is activated by IHF S in stationary-phase .
+The dps promoter is activated by IHF in stationary-phase .
+The dps promoter is activated by IHF S in stationary-phase .
+The dps promoter is activated by IHF in stationary-phase .
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+The fact that tnpA inhibited InvF protein expression at an early growth phase while not affecting invF mRNA levels suggests that translation inhibition is invF pairing .
+The fact that tnpA inhibited InvF protein expression at an early growth phase while not affecting invF mRNA levels suggests that translation inhibition is at least one consequence of tnpA .
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+Expression of the SPI-1 master regulatory gene hilA and five HilA-regulated SPI-1 genes ( sipB , spaO , invH , prgH and invF ) was tested in the loiA mutant , in comparison with the wild-type strain , grown under SPI-1-inducing conditions ( low O2 , high salt ) .
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+To test for the specificity of RflM in promoting RcsB-dependent repression of flhDC , we analyzed the transcript levels of various RcsB targets in the absence or presence of rflM ing to the RcsCDB regulon were regulated by RcsB independently of the presence of RflM .
+To test for the specificity of RflM in promoting RcsB-dependent repression of flhDC , we analyzed the transcript levels of various RcsB targets in the absence or presence of rflM ing to csgD were regulated by RcsB independently of the presence of RflM .
+To test for the specificity of RflM in promoting RcsB-dependent repression of flhDC , we analyzed the transcript levels of various RcsB targets in the absence or presence of rflM ing to dps were regulated by RcsB independently of the presence of RflM .
+To test for the specificity of RflM in promoting RcsB-dependent repression of flhDC , we analyzed the transcript levels of various RcsB targets in the absence or presence of rflM ing to wzzB were regulated by RcsB independently of the presence of RflM .
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+In addition to HilD , the expression of lpxR in SPI-1-inducing conditions is positively regulated by a MarR-like regulator63 .
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+In contrast , H-NS positively regulates OmpF levels by transcriptionally repressing micF .
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+RT-PCR analysis independently showed an NO-dependent downregulation in the transcription of PhoP-activated genes phoP , phoQ , mig-14 and phoN , while RNS treatment did not affect ( e.g. , rpoD ) or even increased ( e.g. , hmpA ) the expression of other loci ( fig. 5B ) .
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+Although not significantly enriched within the set of directly PhoPQ-regulated genes , the functional class related to pathogenicity and virulence also contained potential PhoPQ-dependent targets ( pagC , mgtC , virK , and STM0306 ) .
+STM0306 , a fourth PhoPQ-regulated gene that is involved in pathogenicity , is a paralog of the S. typhimurium SapA protein , which was shown to play a role in virulence ( Parra-Lopez et al. 1993 ) .
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+LeuO has also been shown to repress the acid stress regulator cadC in E. coli
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+However , translational regulator for flhD expression in E. coli in z66 revealed that OmpR did condition .
+However , translational regulator for flhD expression in E. coli in the high-osmolarity expression investigation of fljB revealed that OmpR did condition .
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+List of genes Description List of genes Description DNA-binding transcriptional dual regulator , global regulator of anaerobic-growth spaM Needle complex assembly protein fnr Type III secretion apparatus protein Needle complex export protein hilA fliA Invasion protein transcriptional activator RNA polymerase , sigma-28 factor invG invA Putative regulatory protein for type III secretion apparatus Type III secretion low calcium response chaperone LcrH/SycD ATP-dependent Clp protease proteolytic subunit invF clpP Needle complex pathogenicity 1 island effector Description for the genes in Figure 11b .
+List of genes Description List of genes Description DNA-binding transcriptional dual regulator , global regulator of anaerobic-growth spaM Needle complex assembly protein fnr Type III secretion apparatus protein Needle complex export protein hilA fliA Invasion protein transcriptional activator RNA polymerase , sigma-28 factor invG invA Putative regulatory protein for type III secretion apparatus Type III secretion low calcium response chaperone LcrH/SycD ATP-dependent Clp protease proteolytic subunit invF clpP Needle complex inner membrane protein Description for the genes in Figure 11b .
+List of genes Description List of genes Description DNA-binding transcriptional dual regulator , global regulator of anaerobic-growth spaM Needle complex assembly protein fnr Type III secretion apparatus protein Needle complex export protein hilA fliA Invasion protein transcriptional activator RNA polymerase , sigma-28 factor invG invA Putative regulatory protein for type III secretion apparatus Type III secretion low calcium response chaperone LcrH/SycD ATP-dependent Clp protease proteolytic subunit invF clpP Needle complex pathogenicity 1 island effector protein sicA/spaT prgH Surface presentation of antigens protein SpaS Invasion-associated .
+List of genes Description List of genes Description DNA-binding transcriptional dual regulator , global regulator of anaerobic-growth spaM Needle complex assembly protein fnr Type III secretion apparatus protein Needle complex export protein hilA fliA Invasion protein transcriptional activator RNA polymerase , sigma-28 factor invG invA Putative regulatory protein for type III secretion apparatus Type III secretion low calcium response chaperone LcrH/SycD ATP-dependent Clp protease proteolytic subunit invF clpP Needle complex inner membrane protein protein sicA/spaT prgH Surface presentation of antigens protein SpaS Invasion-associated .
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+For SPI3 , the PhoP-activated mgtCBR operon [ 40 ] was up-regulated > 15 fold within mac-rophages , while other SPI3 genes ( slsA , marT and rhuM ) were moderately up-regulated .
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+The pagD and pagC genes are PhoP-activated genes ( 9 ) located next to each other in the Salmonella chromosome but transcribed in opposite directions from a shared intergenic region .
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+Schematic diagram _ illustrating the interplay between STM1344 in the regulation of FlhD4C2 functionality
+STM1344 suppress the functionality of the master regulator of the flagella regulatory cascade , FlhD4C2 .
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+PhoPQ-regulated genes include lpxO , whose product results in the addition of 2-hydroxymyristate to the 3 = position of lipid-A ( A ) ; pagL , whose product results in deacylation at the 3 = position of lipid-A ( B ) ; and pagP , whose product results in the addition of a palmitate chain to the 2 = position of lipid-A ( C ) .
+Other genes of interest include pagP , a PhoPQ-regulated palmitoyl transferase for lipid-A ; sdiA , a regulator of quorum-sensing and virulence ( Ahmer et al. 1998 ; Volf et al. 2002 ) ; permeases of oligopeptides , such as oppF and oppB ( Goodell and Higgins 1987 ; Orchard and Goodrich-Blair 2004 ) ; and several genes involved in drug resistance , such as emrE and nudF .
+Other genes of interest include pagP , a PhoPQ-regulated palmitoyl transferase for lipid-A ; a regulator of virulence ; permeases of oligopeptides .
+Other genes of interest include pagP , a PhoPQ-regulated palmitoyl transferase for lipid-A ; a regulator of quorum-sensing ; permeases of oligopeptides .
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+We evaluated the utilities of these vectors by fusing the-helix domains of PspA and pneumococcal surface protein C ( PspC ) , to bla SS under the control of the Ptrc promoter .
+We evaluated the utilities of these vectors by fusing the-helix domains of pneumococcal surface protein A and pneumococcal surface protein C ( PspC ) , to bla SS under the control of the Ptrc promoter .
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+Transcription of katN is RpoS and growth phase dependent Salmonella strains carrying the Tn5B21 inserts G57 and I28 were initially selected because they contain RpoSregulated lacZ gene fusions ( Ibanez-Ruiz et al. , 2000 ) .
+Thirty-eight unique mutants _ carrying transcriptional lacZ gene fusions positively regulated by RpoS
+Vijayakumar , S.R. , Kirchhof , M.G. , Patten , C.L. , and Schellhorn , H.E. ( 2004 ) RpoS-regulated genes of Escherichia coli identified by random lacZ fusion mutagenesis .
+To further examine the SraL regulation by RpoS , we analyzed sraL promoter response in a transcriptional-fusion to lacZ reporter gene in both rpoS mutant genetic backgrounds .
+To further examine the SraL regulation by RpoS , we analyzed sraL promoter response in a transcriptional-fusion to lacZ reporter gene in both wild-type .
+Vijayakumar SRV , Kirchhof MG , Patten CL & Schellhorn HE ( 2004 ) RpoS-regulated genes of Escherichia coli identified by random lacZ fusion mutagenesis .
+RpoS-regulated genes of Escherichia coli identified by random lacZ fusion mutagenesis .
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+The expression of ilvIH gene products is inhibited by leucine , apparently due to a requirement for Lrp for activation of ilvIH transcription .
+The expression of AHAS III is inhibited by leucine , apparently due to a requirement for Lrp for activation of ilvIH transcription .
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+In summary , we have shown that the H-NS-mediated regulation of hlyE expression in E. coli K-12 is more complex than was previously suggested because H-NS can negatively to hlyE expression .
+In summary , we have shown that the H-NS-mediated regulation of hlyE expression in E. coli K-12 is more complex than was previously suggested because H-NS can contribute positively .
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+Expression of ptsG , is repressed by Mlc .
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+Activated OxyR induces katG , dps ahpCF .
+Activated OxyR induces katG , dps lipids .
+Activated OxyR induces katG , DNA-protection ahpCF .
+Activated OxyR induces katG , DNA-protection lipids .
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+sifB is regulated by SprB
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+The ugtL gene mediates polymyxin B resistance independently of the PmrA-PmrB system phoP Salmonella are > 20 times more polymyxin sensitive than a pmrA mutant when bacteria are grown in low ygjU 3394555 3392617 rfaB rfaI 3914096 3915562 slsA STM3760 cigR 3959077 3960805 rhaT rhaR 4260472 4262386 STM0725 STM0726 STM0724 792487 790384 Mg2 + ( Wosten et al. , 2000 ) , indicating that a PmrA-inde-pendent PhoP-regulated gene ( s ) is necessary for poly-myxin resistance .
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+The promoters of gatY are negatively regulated by GatR .
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+SlyA is also involved in the regulation of mig-14
+The mig-14 genes appear to be regulated by both SlyA , by a mechanism .
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+Effect of lrp mutations on the expression of traJ transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the regulatory genes traJ and finP .
+Effect of lrp mutations on the expression of finP transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the regulatory genes traJ and finP .
+Effect of lrp mutations on the expression of tra transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the regulatory genes traJ and finP .
+Effect of lrp mutations on the expression of traJ transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the first gene of the tra operon , .
+Effect of lrp mutations on the expression of traJ transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of traY , .
+Effect of lrp mutations on the expression of finP transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the first gene of the tra operon , .
+Effect of lrp mutations on the expression of finP transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of traY , .
+Effect of lrp mutations on the expression of tra transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of the first gene of the tra operon , .
+Effect of lrp mutations on the expression of tra transcriptional units To identify the promoter regulated by Lrp in the transfer regulon of pSLT , we investigated the effect of lrp mutations on the expression of traY , .
+that Lrp could bind to the lrp regulatory region in the absence of amino-acids
+It has been shown previously that leucine does not alter the binding of Lrp to the regulatory region of the E. coli lrp gene .
+The modifications to the patterns of hypersensitivity seen in the lrp regulatory region in the presence and absence of leucine are consistent with an adjustment to the Lrp -- DNA contacts due to the influence of the amino-acid on Lrp protein structure .
+The modifications to the patterns of protection seen in the lrp regulatory region in the presence and absence of leucine are consistent with an adjustment to the Lrp -- DNA contacts due to the influence of the amino-acid on Lrp protein structure .
+The effect of adding leucine is not to remodel it so that the negative influence of the Lrp protein on lrp promoter function is attenuated .
+The effect of adding leucine is not to abolish DNA interaction so that the negative influence of the Lrp protein on lrp promoter function is attenuated .
+The effect of adding leucine is not to abolish Lrp so that the negative influence of the Lrp protein on lrp promoter function is attenuated .
+( A ) The mRNA levels of Lrp-regulated genes in chromosome lrp mutants .
+The chromosome K36Q , K36R , of Lrp-regulated genes in chromosome lrp mutants .
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+that hcp transcription is activated by S-nitrosylation of OxyR during anaerobic nitrate respiration
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+These results suggest that the induction of sifB expression by acidic pH inside the vacuole is mediated by both B and OmpR -- EnvZ .
+These results suggest that the induction of sifB expression by acidic pH inside the vacuole is mediated by both SsrA and OmpR -- EnvZ .
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+PmrA has been shown to bind the promoters of other PmrA-regulated loci , including pmrCAB , pmrHFIJKLM , and pmrE ( ugd ) ( 1 , 56 ) .
+Several PmrA-regulated loci involved in modification of LPS have been identified , including pmrE ( pagA , ugd ) , which encodes a putative UDP-glucose dehydrogenase , and the pmrHFIJKLM operon ( 17 ) .
+PmrA has been shown to bind ugd .
+Results Mutation of the tolB locus promotes ugd transcription in a phoP-and pmrA-independent manner The ugd gene product participates in multiple cellular activities , suggesting that regulatory systems other than PhoP -- PmrA -- PmrB might also control ugd expression .
+Collectively , these results strongly suggest that the pmrC , ugd and pmrG genes and the pbgPE operon are the only PmrA-regulated determinants required for Fe ( III ) resistance .
+The absence of transcriptional linkage between the RpoN and the PmrA regulons was corroborated because no significant differences were observed when the expression of PmrAcontrolled genes ( pmrI , pmrC , pmrF , and ugd ) was compared either in a RpoN or in a 1 DrpoN strain grown in LB ( exponential or stationary-phase ) or in a low-Mg N-21 minimal-medium , which are PhoP-and PmrA-inducing conditions ( Soncini & Groisman , 1996 ) ( Fig. 3a and data not shown ) .
+( a ) b-Galactosidase activities were determined for pmrI : : MudJ , pmrC : : MudJ , pmrF : : MudJ and ugd : : MudJ ( all PmrA-regulated genes ) in an rpoN ( W-1 t ) or in a DrpoN strain .
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+PhoPQ , seem to convert pH decreases into the regulation of different virulence-factors while the primary role of fur appears to be protection against acid stress itself .
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+Previous studies have shown that CpxR-P activates the expression of the cpxRA operon .
+CpxR is in agreement with previous studies indicating that CpxR-P induces the expression of the cpxRA operon
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+Our results indicate that only the PmrA regulator binds to the wzz promoter , inducing fepE gene expression .
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+In Salmonella enterica , overexpression of the RstA protein lowered the levels of the alternative sigma factor RpoS by an unknown mechanism , which consequently downregulated transcription of three RpoS-controlled genes , narZ , spvA , and bapA , in stationary-phase ( 4 ) .
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+-RRB- , narG -LRB- are positively regulated by SlyA
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+Inactivation of LsrR by the presence of phosphorylated AI-2 allows invF , sicA , sopB , sopE and fliC , fliD gene transcription .
+Inactivation of LsrR by the presence of phosphorylated AI-2 allows invF , sicA , sopB , sopE and flagella gene transcription .
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+DNA damage has been shown to be sufficient to stimulate umuC transcription and the SOS response .4,5 The initial response to DNA damage is induction of LexA repressed genes .2,3 -LRB- In Escherichia .
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+S1 ) and that the ssrB promoter mutation had no effect on the expression of the PmrA-activated pmrC gene ( Fig. 5C ) .
+a posttranslational activator of PmrA represses ssrB transcription
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+HilA binds the promoter of ssaH
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+Strain FeCl3 MIC ( mM ) 3200-100-1600-100 1600-100-1600 Wild-type DpmrAB/vector DpmrAB/ppmrG DpmrAB DpmrAB rfaY DpmrC ugd pmrG DpmrC ugd pmrG rfaY Modification of the Hep ( I ) phosphate with phosphoethanolamine is not required for Fe ( III ) resistance The core region of the LPS has two phosphates : one at Hep ( II ) that is targeted by PmrG ( Fig. 2C ) , and one at Hep ( I ) that can be modified with phosphoethanolamine by the PmrA-activated cptA gene product ( Tamayo et al. , 2005 ) .
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+NsrR regulation of tehAB was not observed
+Previous studies indicated that NsrR binds to the promoter region of tehAB
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+Real-time PCR analysis revealed that upon RstA expression , transcriptional repression of the fhuF gene by the FLAG-tagged Fur protein was as efficient as in the strain with the wild-type Fur protein ( see Fig .
+The feoB deletion prevented the RstA-promoted repression of transcription levels of fhuF .
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+We reason that metE is not a true target of AI-2 regulation but , instead , metE transcription is induced in the wild-type luxS strain relative to the luxS null strain because homocysteine is produced during the generation of AI-2 in the LuxS strain .
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+However , unlike spf -- CRP complex , cyaR is activated by CRP .
+However , unlike spf -- CRP complex , cyaR is activated by CRP .
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+It is possible that the downregulation of sefA in TSP-adapted cells may result from the upregulation of RpoS because RpoS is a negative regulator of sefA expression .
+It is possible that the upregulation of spvR may result from the upregulation of RpoS because RpoS is a negative regulator of sefA expression .
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+Of 93 CsrA-induced genes identified in-vitro , we found that 88 % were downregulated during infection of J774A .1 macrophages by S. typhimurium ; consistent with this , csrA was also downregulated threefold ( Figure 1 ) [ 19,30 ] .
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+RcsA-RcsB-regulated genes are primarily involved in exopolysaccharide ( EPS ) production and include the 19-gene colanic acid capsular operon and the yjbEFGH operon , which encodes the biosynthesis of a distinct EPS ( 18 , 19 ) .
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+In turn , fliA is positively controlled by the gene products FlhD .
+The FlhD proteins act together in an FlhD2C2 hetero-tetramer to activate the σ70 promoter of fliA gene .
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+P-galac-tosidase activities were determined in a constitutively derepressed crp mutant background in order to quantitate promoter activities independent of regulation by CAMP-CRP -LRB- the results were unaffected by addition of CAMP-data not shown -RRB- .
+Therefore , overproduction of cAMP by crp mutants must be the indirect consequence of a defect in CRP-mediated regulation of adenylate cyclase activity rather thancya expression , a conclusion .
+Therefore , overproduction of cAMP by crp mutants must be the direct consequence of a defect in CRP-mediated regulation of adenylate cyclase activity rather thancya expression , a conclusion .
+Mechanism of the down-regulation of cAMP-receptor-protein by glucose in Escherichia coli : role of autoregulation of the crp gene .
+One possible route would be regulation of crp by SdsR , for CRP-deficient Salmonella display altered susceptibility to antibiotic challenge .
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+Among the SPI-5 genes , primer-extension analysis revealed that sopB were induced at entry into the stationary-phase under standard growt conditions independently of RpoS .
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+In contrast , the H-NSI11A mutant main-Disruption of the Hha/H-NS Interaction in Vivo Results in tained wild type levels of proV transcript but derepressed hilA Misregulation of Select H-NS-repressed Genes -- To clarify and ssrA by 145-and 9.5-fold compared with H-NSWT levels .
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+Additionally , transcription of many genes in SPI-1 declined in Δpat , including the prg ( PhoP-repressed products ) genes prgK , prgJ , prgI , and prgH ( to ) , encoding component of the needle complex ; the sip ( Salmonella invasion protein ) genes sipA , sipD , sipC , and sipB ( approximately ) , encoding translocation machinery component ; and the inv ( invasion ) genes invJ , invI , invC , invB , invA , invE , invG , invF , and invH ( approximately ) , which were essential for invasion of cells ( Supplementary Table 4 ) .
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+To investigate the mechanism underlying the expressional regulation of fljB : z66 , gene deletion mutants of the regulators FliA were constructed in this study .
+To investigate whether fljB is regulated by FliA like other biphasic S. fliA mutants were affected by the osmotic environment , an ompR mutant was also prepared .
+To investigate whether fljB is regulated by FliA like other biphasic S. flhDC mutants were affected by the osmotic environment , an ompR mutant was also prepared .
+To investigate whether fljB is regulated by FliA like other biphasic S. enterica mutants were affected by the osmotic environment , an ompR mutant was also prepared .
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+These results agree well with those for the proU operon when H-NS binds within the proV operon .
+the H-NS-regulated proU operon where H-NS binds to downstream-regul-atory element within the proV structural gene
+the H-NS-regulated proU operon where H-NS binds to the DRE within the proV structural gene
+four H-NS _ regulated proV
+the hemX gene were used as negative control regions , respectively , as H-NS binds to the proV promoter .
+the hemX gene were used as positive control regions , respectively , as H-NS binds to the proV promoter .
+The proV promoter were used as negative control regions , respectively , as H-NS binds to the proV promoter .
+The proV promoter were used as positive control regions , respectively , as H-NS binds to the proV promoter .
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+The two-component regulatory OmpR/EnvZ function through HilD , thus inducing invF .
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+As OmpR also controls the expression of the acid-induced virulence operon ssrAB , acid shock induction of ompR was examined to gain insight into how Salmonella links virulence with survival at extreme acid-pH .
+In this paper , we examine the details of ompR induction by the potential roles of alternative OmpR phosphodonors in acid tolerance .
+OmpR _ serving as an activator of ompR transcription during P1 , transcript
+OmpR _ serving as an activator of ompR transcription during the P2
+OmpR _ serving as an activator of ompR transcription during acid shock
+A radiolabelled ompR promoter DNA fragment were incubated with increasing quantities of OmpR -LRB- as indicated -RRB- for 2 h at room temperature .
+A. Western blot analysis of OmpR was used to examine the effect of hns on the acid shock induction of ompR .
+As OmpR also controls the expression of the acid-induced virulence operon ssrAB , acid shock induction of ompR was examined to gain insight into how Salmonella links virulence with survival at extreme acid-pH .
+In this paper , we examine the details of ompR induction by the potential roles of alternative OmpR phosphodonors in acid tolerance .
+OmpR _ serving as an activator of ompR transcription during P1 , transcript
+OmpR _ serving as an activator of ompR transcription during the P2
+OmpR _ serving as an activator of ompR transcription during acid shock
+A radiolabelled ompR promoter DNA fragment were incubated with increasing quantities of OmpR -LRB- as indicated -RRB- for 2 h at room temperature .
+A. Western blot analysis of OmpR was used to examine the effect of hns on the acid shock induction of ompR .
+CadC interacts directly with OmpR Since S. enterica serovar Typhimurium OmpR response re-gulator was shown to induce its own synthesis by binding to its promoter ( Bang et al. , 2002 ) , we hypothesized that CadC could mediate the repression of ompR gene expression by direct interaction with OmpR , sterically hindering binding of OmpR to its own promoter or RNA polymerase .
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+This result indicated that H-NS was functioning to repress csgD .
+This work clearly shows that , as observed in E. coli , H-NS represses expression of csgD in Salmonella .
+our earlier observations H-NS repressed expression of csgD
+Furthermore , we identify H-NS as a repressor of csgD in Salmonella , instead of an activator .
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+Other genes of interest include pagP , a PhoPQ-regulated palmitoyl transferase for lipid-A ; sdiA , a regulator of quorum-sensing and virulence ( Ahmer et al. 1998 ; Volf et al. 2002 ) ; permeases of oligopeptides , such as oppF and oppB ( Goodell and Higgins 1987 ; Orchard and Goodrich-Blair 2004 ) ; and several genes involved in drug resistance , such as emrE and nudF .
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+Inactivation of Crl , results in reduced expression of csgD biofilm-related genes .
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+in kb ) of salmonellae aspV ( 304.7 ) GEI 0266/0307 ( SPI-6 ) 46.7 42 52.3 STM0272 , STM0291 , safC , sinR STM0274A ( invasol ) , STM0284 ( putative shiga-like toxin A subunit ) , STM0306 ( SlyA-activated ; homologue to sapA involved in resistance to antimicrobial peptides and homologue to putative invasin pagN ) , STM307 ( homologue to Shigella VirG protein ) 51.1 STM1031 , STM1033 , STM1041 , STM1042 pncB ( 1098.2 ) 45.5 52 GEI 1005/1056 ( Gifsy-2 ) STM1044 ( sodC ) , STM1055 ( gtgE , SlyA-activated ) , STM1056 ( msgA homologue ) 47.2 1672 , 1677 orf ( 1757.9 ) 14.0 14 orf ( 2099.7 ) 36.3 40 GEI 1664/1678 GEI 2016/2058 STM1669 ( invC homologue ) 54.8 cobS , pocR , pduK orf ( 2729.0 ) 47.8 53 GEI 2584/2636 ( Gifsy-1 ) 51.6 STM2585A , STM2589 , STM2585 ( pagJ , SlyA-activated gene ; STM2595 , gipA , STM2603 , Navarre et al. , 2005 ) STM2605 , STM2633 52.1 STM2781 ( virK ) fljA ( 2912.6 ) 34.3 19 GEI 2770/2788 STM2780 ( pipB2 ; Navarre et al. , 2005 ) , mig-14 Fig. 3 .
+in kb ) of salmonellae aspV ( 304.7 ) GEI 0266/0307 ( SPI-6 ) 46.7 42 52.3 STM0272 , STM0291 , safC , sinR STM0274A ( invasol ) , STM0284 ( putative shiga-like toxin A subunit ) , STM0306 ( SlyA-activated ; homologue to sapA involved in resistance to antimicrobial peptides and homologue to putative invasin pagN ) , STM307 ( homologue to Shigella VirG protein ) 51.1 STM1031 , STM1033 , STM1041 , STM1042 pncB ( 1098.2 ) 45.5 52 GEI 1005/1056 ( Gifsy-2 ) STM1044 ( sodC ) , STM1055 ( gtgE , SlyA-activated ) , STM1056 ( msgA homologue ) 47.2 1672 , 1677 orf ( 1757.9 ) 14.0 14 orf ( 2099.7 ) 36.3 40 GEI 1664/1678 GEI 2016/2058 STM1669 ( invC homologue ) 54.8 cobS , pocR , pduK orf ( 2729.0 ) 47.8 53 GEI 2584/2636 ( Gifsy-1 ) 51.6 STM2585A , STM2589 , STM2585 ( pagJ , SlyA-activated gene ; STM2595 , gipA , STM2603 , Navarre et al. , 2005 ) STM2605 , STM2633 52.1 STM2781 ( virK ) fljA ( 2912.6 ) 34.3 19 GEI 2770/2788 STM2780 ( pipB2 ; Navarre et al. , 2005 ) , mig-14 Fig. 3 .
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+moreover , we demonstrate that CpxR-P negatively affects the stability of HilD and thus decreases the expression of HilD-target genes hilA , located in SPI-1 .
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+The isogenic phoP tolC strain showed intermediate permeability , as expected from the fact that some of the PhoPQ-regulated modification reactions , especially the palmitoylation of lipid-A , occur in the wild-type strain to a considerable extent ( 21 ) .
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+LacI whose expression is under the control of the araC PBAD system
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+pmrG are both transcriptionally activated by PmrAB .
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+29 pagC survival pagD pagK PhoPQ-regulated 0 ?
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+this effect was reflected by induction of cspB and proteins ( CspE ) in response to preadaptation to cold-stress
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+Thus , it is possible that AraC regulates transcription from the site within sseD under conditions .
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+Therefore , we compared the transcription of HilD-regulated genes in eK297R and eWT in the lon deletion background , which excludes the effect of protein stability , and found that the messenger RNA levels of HilD-regulated genes in eK297R increased dramatically compared with these in eWT ( Figure 3D ) , indicating that K297R mimicking deacetylation can effectively activate HilD-regulated genes by increasing its DNA-binding affiffinity in the lon mutant background in-vivo .
+Therefore , we compared the transcription of HilD-regulated genes in eK297R and eWT in the lon deletion background , which excludes the effect of protein stability , and found that the messenger RNA levels of HilD-regulated genes in eK297R increased dramatically compared with these in eWT ( Figure 3D ) , indicating that K297R mimicking deacetylation can effectively activate HilD-regulated genes by increasing its DNA-binding affiffinity in the lon mutant background in-vivo .
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+inactivation of narL did not reduce growth in the intes-tinal lumen , although NarL regulates metabolic genes
+inactivation of narL did not reduce growth in the intes-tinal lumen , although NarL regulates a variety
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+While the functions of STM2180 are uncharacterized , MetR is known to be involved in the regulation of methionine biosynthesis .
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+Besides the putative ` rck operon 
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+Another ` Fur-activated 
+These data suggest that Fur activates SPI1 in a manner different from that of Fur activation of sodB .
+One such `` Fur-activated 
+Known `` Fur-activated 
+Fur activates sodB by repressing the expression of ryhB under high-iron conditions .
+Thus , Fur positively controls sodB at the posttranscriptional level .
+In E. coli , expression of sodB is activated by Fur via repression of the small RNA RyhB .
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+These results show that HilD positively controls the expression of the sinR genes , independently of InvF .
+These results show that HilD positively controls the expression of the sinR genes , independently of HilA .
+HilD induces the expression of sinR , in the absence of other Salmonella-specific regulators .
+Thus , HilD positively regulates the expression of the sinR genes , and positively .
+HilD positively regulates sinR in S. Typhimurium .
+HilD induces the expression of sinR , in E. coli MC4100 .
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+an hfq-ompR double mutant were used to determine whether the regulation of tviA expression by Hfq is associated with the OmpR-EnvZ system .
+An ompR mutant double mutant were used to determine whether the regulation of tviA expression by Hfq is associated with the OmpR-EnvZ system .
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+PmrA-regulated loci identified included dgoA and yibD and demonstrated 500-and 2,500-fold activation by PmrA , respectively .
+The remaining PMs mutants ( surA and tolB ) , as well as the two PmrA-regulated gene ( yibD and dgoA ) mutants , retained aminoarabinose on lipid-A .
+The PmrA-regulated gene mutants JSG897 ( yibD ) and JSG899 ( dgoA ) were also analyzed for sensitivity to PM by MIC assay .
+Mutants identified in the MudJ transposon mutagenesis screen Tn insertion site Description Strain PM sensitive imp/surA tolB gnd gnd yibD dgoA pmrC pmrC pmrC pmrC pmrI pmrI 851 895 JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG 1272-1290-897-899 901-918-973-1036 923 925 PmrA regulated PmrA regulated , PM sensitive PmrA-regulated genes identified in the screen in iron resistance , JSG897 ( yibD ) and JSG899 ( dgoA ) were grown on solid N-minimal-medium supplemented with 100 M FeSO4 .
+Mutants identified in the MudJ transposon mutagenesis screen Tn insertion site Description Strain PM sensitive imp/surA tolB gnd gnd yibD dgoA pmrC pmrC pmrC pmrC pmrI pmrI 851 895 JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG JSG 1272-1290-897-899 901-918-973-1036 923 925 PmrA regulated PmrA regulated , PM sensitive PmrA-regulated genes identified in the screen in iron resistance , JSG897 ( yibD ) and JSG899 ( dgoA ) were grown on solid N-minimal-medium supplemented with 100 M FeSO4 .
+For further characterization of the PmrA-regulated gene mutants , the promoter regions of yibD and dgoA were analyzed for the presence of a putative PmrA-binding site , which was defined by the occurrence of the consensus binding sequence for PmrA , YTTAAK-N5-YTTAAK ( 1 ) .
+yibD , dgoA , and gnd ( likely affecting pmrE ) played no role in PmrA-regulated resistance to high iron concentrations , while surA and tolB mutations grew poorly on high iron media .
+JSG897 and JSG899 , with mutations in PmrA-regulated genes yibD and dgoA , respectively , also still possessed Ara4N modification of lipid-A in similar amounts to the parental PmrAc strain .
+PmrA-regulated gene mutants JSG1525 ( yibD ) and JSG1526 ( dgoA ) were as virulent as wild-type Salmonella serovar Typhimurium , so the genes interrupted have no essential role in the infection process ( Table 4 ) .
+All PMs mutants identified in this study demonstrated a defect in virulence compared to wild-type Salmonella serovar Typhimurium when administered orally to mice , while the PmrA-regulated gene ( yibD and dgoA ) mutants showed normal virulence in mice .
+Sequencing of the MudJ insertion site of JSG899 identified dgoA as a PmrA-regulated gene .
+While it is possible that these PmrA-regulated genes ( as well as the genes involved in PM resistance ) could affect the other known PmrA-induced LPS modification , pEtN , we feel that this is unlikely based on what is known about the identified genes ( surA , tolB , and pmrE ) and because yibD and dgoA do not affect virulence or PM resistance , which are predicted phenotypes of the loss of pEtN modification from the core ( 59 ) .
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+Thus , SsrB regulates transcription of sseJ by both relief of H-NS repression .
+Thus , SsrB regulates transcription of sseJ by both direct activation of H-NS repression .
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+Recent studies indicate that HilA binds to specific sequences in the prgH promoters .
+It is known that prgH is under the regulation of HilA .
+Expression of the SPI-1 master regulatory gene hilA and five HilA-regulated SPI-1 genes ( sipB , spaO , invH , prgH and invF ) was tested in the loiA mutant , in comparison with the wild-type strain , grown under SPI-1-inducing conditions ( low O2 , high salt ) .
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+It is likely the effects of σE on SPI-2 transcription is mediated by SsrB because Sly , can complement the decrease of SPI-2 expression as a result of rpoE deletion .
+It is likely the effects of σE on SPI-2 transcription is mediated by SsrB because overexpression of Ssr , can complement the decrease of SPI-2 expression as a result of rpoE deletion .
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+One HilD-activated gene product , acts to repress flhDC transcription , providing a feedback loop for the entire fla-gellar-Spi1 regulon .
+Posttranscriptional activation of flhDC occurs at the level of the flagellar regulator FliZ via regulation of HilD activity and repression of the antiFlhD4C2 factor YdiV .
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+kdgM -LRB- encoding oligogalacturonate-specific porin -RRB- appear to be most strongly controlled by KdgR , while kdgK , araH , are controlled by additional regulators .
+Genes kduI -LRB- encoding 4-deoxy-L-threo-5-hexosulose-uronate ketol-isomerase -RRB- appear to be most strongly controlled by KdgR , while kdgK , araH , are controlled by additional regulators .
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+In low-Mg2 + environment -LRB- extracytoplasmic Mg2 + -RRB- , the PhoPQ two-component systems directly activates mgtA transcription .
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+Efforts in our laboratory to demonstrate binding of purified HilE protein to the hilA promoter have failed , however , recent work demonstrated that the HilE protein interacts with HilD , using a bacterial two-hybrid assay .
+colleagues have identified HilE as a negative regulator of hilA transcription .
+Jones have identified HilE as a negative regulator of hilA transcription .
+In E. coli , a hilA was regulated by HilE only when HilD protein was present .
+Also , when hilD is under the control of the lac promoter , hilA is still regulated by HilE .
+Also , when hilD is under the control of the lac promoter , hilA is still regulated by HilE .
+To determine the effects of HilE on the regulation of hilA via PhoPQ , we conducted a-galactosidase assay .
+To determine the effects of HilE on the regulation of hilA via PhoPQ , we conducted lacZY expression .
+Fahlen et al. identified HilE as a negative regulator of hilA transcription provided bacterial two-hybrid data .
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+the control of the DnaA binding to oriC can be related with the partial reestablishment of the replication asynchrony _ observed at every seqA mutant
+the control of the DnaA binding to oriC in-vitro _ observed at every seqA mutant
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+H-NS-deficient mutants strongly increased RpoS due to enhanced rpoS translation .
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+The OmpR/EnvZ two-component regulatory system regulates the porin genes ompF to changes in osmolarity .
+In S. Typhi , the OmpR/EnvZ system is involved in the regulation of ompF porin genes , where both OmpF are expressed as abundant outer-mem-brane proteins as in E. coli .
+In S. Typhi , the OmpR/EnvZ system is involved in the regulation of ompF porin genes , where both OmpC are expressed as abundant outer-mem-brane proteins as in E. coli .
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+As the Ipro values of spvR regulatory mutants were lower than those of phoP mutants , we investigated whether the function of these proteins as negative regulators of bacterial intracellular growth was dependent on the PhoP-PhoQ system .
+As the Ipro values of rpoS regulatory mutants were lower than those of phoP mutants , we investigated whether the function of these proteins as negative regulators of bacterial intracellular growth was dependent on the PhoP-PhoQ system .
+As the Ipro values of slyA regulatory mutants were lower than those of phoP mutants , we investigated whether the function of these proteins as negative regulators of bacterial intracellular growth was dependent on the PhoP-PhoQ system .
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+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
+HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB .
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+These results suggest that SlyA controls expression of magainin 2 resistance determinants in addition to the ugtL gene , which appears to be the sole SlyA-regulated gene mediating polymyxin B resistance .
+The polymyxin B susceptibility of the slyA mutant was the same as that exhibited by the ugtL mutant ( Fig. 5A ) and could be complemented to wild-type levels by a plasmid that expressed the ugtL gene from a heterologous promoter ( Fig. 5B ) , suggesting that ugtL is the only SlyA-regulated gene mediating polymyxin B resistance .
+We propose that the SlyA proteins control ugtL transcription .
+that both SlyA proteins bind to the ugtL promoter , suggesting that these two proteins use a feed-forward loop to control ugtL expression
+These results demonstrate that the SlyA proteins bind to the ugtL promoter .
+The SlyA proteins bind to the ugtL promoter .
+These results suggest that SlyA controls expression of magainin 2 resistance determinants in addition to the ugtL gene .
+We have established that transcription of polymyxin B resistance gene ugtL is controlled by the SlyA proteins in what appears to be a feedforward loop design .
+The SlyA protein bound to a region located downstream from the ugtL transcription start site for a regulatory protein -LRB- Fig. 1A -RRB- .
+Taken together with the identification of binding sites for both the SlyA in Fig. 2C , these results support the notion of a feedforward design in the regulation of ugtL transcription .
+Taken together with the identification of binding sites for both the SlyA in the ugtL promoter , these results support the notion of a feedforward design in the regulation of ugtL transcription .
+Model _ illustrating the feed-forward regulation of the ugtL gene by the SlyA proteins
+Transcriptional control of the antimicrobial peptide resistance ugtL gene by SlyA regulatory proteins .
+Transcriptional control of the antimicrobial peptide resistance ugtL gene by SlyA regulatory proteins .
+Consistently , results from different laboratories showed that SlyA regulates a subset of PhoP-dependent genes , including ugtL , in Salmonella .
+The S. Typhimurium ugtL are regulated by a similar mechanism , involving the coordinated actions of SlyA .
+Transcriptional control of the antimicrobial peptide resistance ugtL gene by SlyA regulatory proteins .
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+More recently it has been shown that the leuO gene is activated by the transcriptional regulators RcsB and BglJ .
+the response regulator RcsB activates leuO transcription in conjunction with BglJ , counteracting H-NS repression of leuO transcription
+More recently , it was shown that leuO expression in E. coli can be activated by the RcsB regulators .
+Also , LeuO expression was detected in a phosphate-restricted media ; and recently it was shown that the expression of the leuO gene can be activated by the RcsB HAS SEVERAL FUNCTIONS IN VIVO Even though LeuO is expressed at very low level in standard laboratory conditions , it seems that in-vivo it has a role in bacterial survival .
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+A set of PhoP-regulated loci , including the phoPQ operon , can be found in other enterobacteria such as E. coli , while other pag genes are Salmonella specific ( 31 ) .
+multiple genomes found that the only targets directly regulated by PhoP in all species were the phoPQ operon itself
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