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1.
Fig 6

Fig 6. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

Schematic representation of P. gingivalis mechanisms mediating response to nitrosative stress.

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.
2.
Fig 1

Fig 1. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

Sensitivity of P. gingivalis to nitrosative stress. P. gingivalis W83 was grown to midlogarithmic phase under anaerobic conditions in mycoplasma broth without hemin and was diluted to an OD660 of 0.1. Various concentrations of nitrite or nitrate (A) (amount given in mM) or GSNO (B) (amount given in mM × 10−3) were added to the cultures. Unsupplemented cultures served as controls. The cultures were then grown for an additional 48 h at 37°C under anaerobic conditions. Means from the experiment performed in triplicate are shown.

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.
3.
Fig 4

Fig 4. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

Role of HcpR on P. gingivalis growth in the presence of nitric oxide. P. gingivalis strains were anaerobically grown to midlogarithmic phase in mycoplasma broth without hemin. The cultures were then diluted to an OD660 of 0.1 in mycoplasma minus hemin, and 1 mM nitrite or 30 nM GSNO was then added to the cultures. Unsupplemented cultures served as controls. The cultures were grown for an additional 18 h at 37°C under anaerobic conditions. Means and standard deviations from the experiment performed in triplicate are shown (n = 3; results are ± standard error of the mean). Parental W83 strain (A), HcpR-deficient mutant strain (B). *, P < 0.001, W83 versus V2807 under 30 nM GSNO (Student's t test).

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.
4.
Fig 2

Fig 2. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

Bioinformatics analysis of HcpR. (A) Genomic locus of hcpR. Genes and their orientations are denoted by arrows. IGR, intergenic region. (B) Comparison of amino acid sequences of P. gingivalis HcpR (HcpR), Thermatoga maritima CRP-like regulator TM1171 (TM1171), Lactococcus lactis Fnr-like regulator CAB53581 (LAFNR), and Pseudomonas stutzeri DNR CAB40908 (PSDNR). Amino acids identical in other proteins to that found in HcpR are indicated in red. Two amino acids in the helix-turn-helix (HTH) confer specificity of the protein binding to DNA targets (R180 correlates with G3 and Q181 with G6 in HcpR). (C) Structural model of P. gingivalis HcpR. Amino acids 25 to 135 form a CAP motif (ligand-binding motif) and are shown in green, and the HTH region (DNA-binding domain; residues 170 to 210) is designated in yellow. The two domains are separated by a dimerization helix. (D) Structural overlay of HcpR (blue) with PADNR (3dkw) (orange).

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.
5.
Fig 3

Fig 3. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

Roles of HcpR and hemin on P. gingivalis growth in the presence of nitrate or nitrite. P. gingivalis strains were anaerobically grown to midlogarithmic phase in mycoplasma broth without hemin. The cultures were then diluted to an OD660 of 0.1 in mycoplasma minus hemin (−Hm) (A and B) and mycoplasma containing 5 μg/ml hemin (+Hm) (C and D). Various concentrations of nitrite or nitrate (A) were then added to the cultures. Unsupplemented cultures served as controls. The cultures were anaerobically grown for an additional 25 h at 37°C. Means and standard deviations from the experiment performed in triplicate are shown (n = 3; results are ± standard error of the mean). *, P < 0.002, W83 versus V2807 under 1 mM nitrite (Student's t test). Parental W83 strain (A) and HcpR-deficient mutant V2807 strain (B) grown in low hemin conditions (−Hm). W83, V2807, and V2835 (complemented HcpR mutant strain) grown in the presence of high hemin concentrations (+ Hm) with 2 mM (C) and 4 mM (D) nitrite. n = 3; results are ± standard error of the mean.

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.
6.
Fig 5

Fig 5. From: HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells.

P. gingivalis HcpR regulates hcp expression. (A) Organization of the hcp (PG0893) locus. Intergenic sequences (IGS) flank the hcp gene. The HcpR binding site is shown as an orange oval. (B) Bioinformatics analysis of the hcp promoter. The HcpR binding site is shown in orange. The transcriptional start site (ts) is located 29 bp upstream of the translational start site (Met). The primer positions used for the generation of the EMSA probe are shown in italics and are underlined. Positions of primers used for qRT-PCR designated 1R, 2R, and 3R are shown in green, and their direction is indicated by an arrow. (C) EMSA. Lysates prepared from IPTG induced E. coli-pET30 hcpR (lane 2, +i) and IPTG-uninduced E. coli-pET30 hcpR (lane 3,+u), and increasing amounts of rHcpR (lanes 5 to 9) were incubated with a 200-bp DNA fragment containing the hcp promoter (DNA). Reaction mixtures containing DNA only were run as reference controls (lanes 1 and 4). Unlabeled hcp promoter DNA (UDNA) was used as a specific competitor (lanes 7 and 9) (10-fold excess over labeled DNA). rHcpR without (lane 5) and reconstituted with (lanes 6 to 9) hemin was used. Lane 5 contained 30 μg of rHcpR, lanes 6 and 7 contained 10 μg of rHcpR, and lanes 8 and 9 had 30 μg of rHcpR.

Janina P. Lewis, et al. Infect Immun. 2012 September;80(9):3319-3331.

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