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GidA, a tRNA Modification Enzyme, Contributes to the Growth, and Virulence of Streptococcus suis Serotype 2.

Gao T, Tan M, Liu W, Zhang C, Zhang T, Zheng L, Zhu J, Li L, Zhou R - Front Cell Infect Microbiol (2016)

Bottom Line: Here, we report a GidA homolog from a Chinese isolate SC-19 of the zoonotic Streptococcus suis serotype 2 (SS2). gidA disruption led to a defective growth, increased capsule thickness, and reduced hemolytic activity.This is consistent with the phenotypes of the mutant.Our findings provide new insight into the regulatory function of GidA in bacterial pathogens.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural UniversityWuhan, China; Veterinary Medicine Laboratory, Institute of Animal Husbandry and Veterinary Science, Hubei Academy of Agricultural ScienceWuhan, China; Wuhan Chopper Biology Co., Ltd.Wuhan, China.

ABSTRACT
Glucose-inhibited division protein (GidA), is a tRNA modification enzyme functioning together with MnmE in the addition of a carboxymethylaminomethyl group to position 5 of the anticodon wobble uridine of tRNA. Here, we report a GidA homolog from a Chinese isolate SC-19 of the zoonotic Streptococcus suis serotype 2 (SS2). gidA disruption led to a defective growth, increased capsule thickness, and reduced hemolytic activity. Moreover, the gidA deletion mutant (ΔgidA) displayed reduced mortality and bacterial loads in mice, reduced ability of adhesion to and invasion in epithelial cells, and increased sensitivity to phagocytosis. The iTRAQ analysis identified 372 differentially expressed (182 up- and 190 down-regulated) proteins in ΔgidA and SC-19. Numerous DNA replication, cell division, and virulence associated proteins were downregulated, whereas many capsule synthesis enzymes were upregulated by gidA disruption. This is consistent with the phenotypes of the mutant. Thus, GidA is a translational regulator that plays an important role in the growth, cell division, capsule biosynthesis, and virulence of SS2. Our findings provide new insight into the regulatory function of GidA in bacterial pathogens.

No MeSH data available.


Related in: MedlinePlus

Mouse infection experiments. (A) Survival curves for mice in experiment infection. Ten mice in each group were separately injected intraperitoneally i with 3 × 109 CFU/mice of SC-19 and ΔgidA. Ten mice were inoculated with saline and served as negative control. Significant difference in survival between different groups were analyzed by Log Rank test (p < 0.05). (B) Bacteria loads in (B) brain, (C) lung, and (D) in spleen. The SC-19 and ΔgidA mutant strains were distinguished by erythromycin added in the TSA plates. Statistical significance was determined by two-tailed t-test (ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001).
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Figure 3: Mouse infection experiments. (A) Survival curves for mice in experiment infection. Ten mice in each group were separately injected intraperitoneally i with 3 × 109 CFU/mice of SC-19 and ΔgidA. Ten mice were inoculated with saline and served as negative control. Significant difference in survival between different groups were analyzed by Log Rank test (p < 0.05). (B) Bacteria loads in (B) brain, (C) lung, and (D) in spleen. The SC-19 and ΔgidA mutant strains were distinguished by erythromycin added in the TSA plates. Statistical significance was determined by two-tailed t-test (ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001).

Mentions: Mice were experimentally infected to detect the role of gidA in S. suis virulence. All of the SC-19-infected mice displayed severe clinical symptoms, such as septicemia and meningitis during 1 dpi, and most of the infected mice (9/10) died during the 7 day observation period. By contrast, the ΔgidA-infected mice exhibited more slight clinical symptoms and low mortality (2/10) (Figure 3A). Therefore, ΔgidA virulence is markedly attenuated.


GidA, a tRNA Modification Enzyme, Contributes to the Growth, and Virulence of Streptococcus suis Serotype 2.

Gao T, Tan M, Liu W, Zhang C, Zhang T, Zheng L, Zhu J, Li L, Zhou R - Front Cell Infect Microbiol (2016)

Mouse infection experiments. (A) Survival curves for mice in experiment infection. Ten mice in each group were separately injected intraperitoneally i with 3 × 109 CFU/mice of SC-19 and ΔgidA. Ten mice were inoculated with saline and served as negative control. Significant difference in survival between different groups were analyzed by Log Rank test (p < 0.05). (B) Bacteria loads in (B) brain, (C) lung, and (D) in spleen. The SC-19 and ΔgidA mutant strains were distinguished by erythromycin added in the TSA plates. Statistical significance was determined by two-tailed t-test (ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001).
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4835480&req=5

Figure 3: Mouse infection experiments. (A) Survival curves for mice in experiment infection. Ten mice in each group were separately injected intraperitoneally i with 3 × 109 CFU/mice of SC-19 and ΔgidA. Ten mice were inoculated with saline and served as negative control. Significant difference in survival between different groups were analyzed by Log Rank test (p < 0.05). (B) Bacteria loads in (B) brain, (C) lung, and (D) in spleen. The SC-19 and ΔgidA mutant strains were distinguished by erythromycin added in the TSA plates. Statistical significance was determined by two-tailed t-test (ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001).
Mentions: Mice were experimentally infected to detect the role of gidA in S. suis virulence. All of the SC-19-infected mice displayed severe clinical symptoms, such as septicemia and meningitis during 1 dpi, and most of the infected mice (9/10) died during the 7 day observation period. By contrast, the ΔgidA-infected mice exhibited more slight clinical symptoms and low mortality (2/10) (Figure 3A). Therefore, ΔgidA virulence is markedly attenuated.

Bottom Line: Here, we report a GidA homolog from a Chinese isolate SC-19 of the zoonotic Streptococcus suis serotype 2 (SS2). gidA disruption led to a defective growth, increased capsule thickness, and reduced hemolytic activity.This is consistent with the phenotypes of the mutant.Our findings provide new insight into the regulatory function of GidA in bacterial pathogens.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural UniversityWuhan, China; Veterinary Medicine Laboratory, Institute of Animal Husbandry and Veterinary Science, Hubei Academy of Agricultural ScienceWuhan, China; Wuhan Chopper Biology Co., Ltd.Wuhan, China.

ABSTRACT
Glucose-inhibited division protein (GidA), is a tRNA modification enzyme functioning together with MnmE in the addition of a carboxymethylaminomethyl group to position 5 of the anticodon wobble uridine of tRNA. Here, we report a GidA homolog from a Chinese isolate SC-19 of the zoonotic Streptococcus suis serotype 2 (SS2). gidA disruption led to a defective growth, increased capsule thickness, and reduced hemolytic activity. Moreover, the gidA deletion mutant (ΔgidA) displayed reduced mortality and bacterial loads in mice, reduced ability of adhesion to and invasion in epithelial cells, and increased sensitivity to phagocytosis. The iTRAQ analysis identified 372 differentially expressed (182 up- and 190 down-regulated) proteins in ΔgidA and SC-19. Numerous DNA replication, cell division, and virulence associated proteins were downregulated, whereas many capsule synthesis enzymes were upregulated by gidA disruption. This is consistent with the phenotypes of the mutant. Thus, GidA is a translational regulator that plays an important role in the growth, cell division, capsule biosynthesis, and virulence of SS2. Our findings provide new insight into the regulatory function of GidA in bacterial pathogens.

No MeSH data available.


Related in: MedlinePlus