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TyrR, the regulator of aromatic amino acid metabolism, is required for mice infection of Yersinia pestis.

Deng Z, Liu Z, He J, Wang J, Yan Y, Wang X, Cui Y, Bi Y, Du Z, Song Y, Yang R, Han Y - Front Microbiol (2015)

Bottom Line: Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene.Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions.In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Sanitary Inspection, School of Public Health, University of South China Hengyang, China ; State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology Beijing, China.

ABSTRACT
Yersinia pestis, the causative agent of plague, poses a serious health threat to rodents and human beings. TyrR is a transcriptional regulator (TyrR) that controls the metabolism of aromatic amino acids in Escherichia coli. In this paper, TyrR played an important role in Y. pestis virulence. Inactivation of tyrR did not seem to affect the in vitro growth of this organism, but resulted in at least 10,000-fold attenuation compared with the wild-type (WT) strain upon subcutaneous infection to mice. In addition, loads of tyrR mutant within mice livers and spleens significantly decreased compared with the WT strain. Transcriptome analysis revealed that TyrR, directly or indirectly, regulated 29 genes encoded on Y. pestis chromosome or plasmids under in vitro growth condition. Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene. Two genes (glnL and glnG) that encode sensory histidine kinase and regulator in a two-component regulatory system involved in nitrogen assimilation were downregulated in the tyrR mutant. Several genes encoding type III secretion proteins were transcribed by 2.0-4.2-fold in a tyrR mutant relative to the WT strain. Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions. In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli. TyrR is a metabolic virulence determinant in Y. pestis that is important for extracellular survival and/or proliferation.

No MeSH data available.


Related in: MedlinePlus

Growth curves of the WT and tyrR mutant strains under two different conditions. Overnight cultures of the WT strain 201 and tyrR mutant were used to inoculate fresh LB broth with pH 5.2 or 7.0. The OD620 values were recorded at fixed time points. Each time point is the average of two measurements and error bars represent standard deviations. The vertical arrows indicate the time point at which samples were removed for RNA extraction.
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Figure 2: Growth curves of the WT and tyrR mutant strains under two different conditions. Overnight cultures of the WT strain 201 and tyrR mutant were used to inoculate fresh LB broth with pH 5.2 or 7.0. The OD620 values were recorded at fixed time points. Each time point is the average of two measurements and error bars represent standard deviations. The vertical arrows indicate the time point at which samples were removed for RNA extraction.

Mentions: Growth of the tyrR mutant was not retarded relative to that of WT strain under the condition used in vitro (Figure 2), indicating that the mutations do not cause any defect in the growth ability. Therefore, the differences in virulence could be due to the specific involvement of this protein under in vivo conditions. We next determine the kinetics of in vivo growth to examine the fitness of Y. pestis WT and tyrR mutant. CI assays were performed by intravenously inoculating the bacterial mixture into mice. The results showed that load burden of WT strain can achieved 107 CFU in the spleen or liver after infection for 48 and 72 h. However, compared with the WT strain, a relatively lower amount bacteria of the tyrR mutant strain was recovered from the spleen or liver. The mean CI values in the spleens were 0.043 at 48 h and 0.003 at 72 h (Figure 3A), and similar CI values were obtained in the livers (0.017 at 48 h and 0.005 at 72 h) (Figure 3B). Clearly, the tyrR mutant was nearly overwhelmed by the population of WT Y. pestis in vivo, indicating that this mutant was much less competitive in vivo than its parental strain.


TyrR, the regulator of aromatic amino acid metabolism, is required for mice infection of Yersinia pestis.

Deng Z, Liu Z, He J, Wang J, Yan Y, Wang X, Cui Y, Bi Y, Du Z, Song Y, Yang R, Han Y - Front Microbiol (2015)

Growth curves of the WT and tyrR mutant strains under two different conditions. Overnight cultures of the WT strain 201 and tyrR mutant were used to inoculate fresh LB broth with pH 5.2 or 7.0. The OD620 values were recorded at fixed time points. Each time point is the average of two measurements and error bars represent standard deviations. The vertical arrows indicate the time point at which samples were removed for RNA extraction.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325908&req=5

Figure 2: Growth curves of the WT and tyrR mutant strains under two different conditions. Overnight cultures of the WT strain 201 and tyrR mutant were used to inoculate fresh LB broth with pH 5.2 or 7.0. The OD620 values were recorded at fixed time points. Each time point is the average of two measurements and error bars represent standard deviations. The vertical arrows indicate the time point at which samples were removed for RNA extraction.
Mentions: Growth of the tyrR mutant was not retarded relative to that of WT strain under the condition used in vitro (Figure 2), indicating that the mutations do not cause any defect in the growth ability. Therefore, the differences in virulence could be due to the specific involvement of this protein under in vivo conditions. We next determine the kinetics of in vivo growth to examine the fitness of Y. pestis WT and tyrR mutant. CI assays were performed by intravenously inoculating the bacterial mixture into mice. The results showed that load burden of WT strain can achieved 107 CFU in the spleen or liver after infection for 48 and 72 h. However, compared with the WT strain, a relatively lower amount bacteria of the tyrR mutant strain was recovered from the spleen or liver. The mean CI values in the spleens were 0.043 at 48 h and 0.003 at 72 h (Figure 3A), and similar CI values were obtained in the livers (0.017 at 48 h and 0.005 at 72 h) (Figure 3B). Clearly, the tyrR mutant was nearly overwhelmed by the population of WT Y. pestis in vivo, indicating that this mutant was much less competitive in vivo than its parental strain.

Bottom Line: Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene.Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions.In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Sanitary Inspection, School of Public Health, University of South China Hengyang, China ; State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology Beijing, China.

ABSTRACT
Yersinia pestis, the causative agent of plague, poses a serious health threat to rodents and human beings. TyrR is a transcriptional regulator (TyrR) that controls the metabolism of aromatic amino acids in Escherichia coli. In this paper, TyrR played an important role in Y. pestis virulence. Inactivation of tyrR did not seem to affect the in vitro growth of this organism, but resulted in at least 10,000-fold attenuation compared with the wild-type (WT) strain upon subcutaneous infection to mice. In addition, loads of tyrR mutant within mice livers and spleens significantly decreased compared with the WT strain. Transcriptome analysis revealed that TyrR, directly or indirectly, regulated 29 genes encoded on Y. pestis chromosome or plasmids under in vitro growth condition. Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene. Two genes (glnL and glnG) that encode sensory histidine kinase and regulator in a two-component regulatory system involved in nitrogen assimilation were downregulated in the tyrR mutant. Several genes encoding type III secretion proteins were transcribed by 2.0-4.2-fold in a tyrR mutant relative to the WT strain. Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions. In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli. TyrR is a metabolic virulence determinant in Y. pestis that is important for extracellular survival and/or proliferation.

No MeSH data available.


Related in: MedlinePlus