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Literatura académica sobre el tema "Streptococcus sanguinis SK36"
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Artículos de revistas sobre el tema "Streptococcus sanguinis SK36"
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Nobbs, Angela H., Yongshu Zhang, Ali Khammanivong y Mark C. Herzberg. "Streptococcus gordonii Hsa Environmentally Constrains Competitive Binding by Streptococcus sanguinis to Saliva-Coated Hydroxyapatite". Journal of Bacteriology 189, n.º 8 (2 de febrero de 2007): 3106–14. http://dx.doi.org/10.1128/jb.01535-06.
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ABSTRACT Competition between pioneer colonizing bacteria may determine polymicrobial succession during dental plaque development, but the ecological constraints are poorly understood. For example, more Streptococcus sanguinis than Streptococcus gordonii organisms are consistently isolated from the same intraoral sites, yet S. gordonii fails to be excluded and survives as a species over time. To explain this observation, we hypothesized that S. gordonii could compete with S. sanguinis to adhere to saliva-coated hydroxyapatite (sHA), an in vitro model of the tooth surface. Both species bound similarly to sHA, yet 10- to 50-fold excess S. gordonii DL1 reduced binding of S. sanguinis SK36 by 85 to >95%. S. sanguinis, by contrast, did not significantly compete with S. gordonii to adhere. S. gordonii competed with S. sanguinis more effectively than other species of oral streptococci and depended upon the salivary film on HA. Next, putative S. gordonii adhesins were analyzed for contributions to interspecies competitive binding. Like wild-type S. gordonii, isogenic mutants with mutations in antigen I/II polypeptides (sspAB), amylase-binding proteins (abpAB), and Csh adhesins (cshAB) competed effectively against S. sanguinis. By contrast, an hsa-deficient mutant of S. gordonii showed significantly reduced binding and competitive capabilities, while these properties were restored in an hsa-complemented strain. Thus, Hsa confers a selective advantage to S. gordonii over S. sanguinis in competitive binding to sHA. Hsa expression may, therefore, serve as an environmental constraint against S. sanguinis, enabling S. gordonii to persist within the oral cavity, despite the greater natural prevalence of S. sanguinis in plaque and saliva.
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El-Rami, Fadi, Kristina Nelson y Ping Xu. "Proteomic Approach for Extracting Cytoplasmic Proteins from Streptococcus sanguinis using Mass Spectrometry". Journal of Molecular Biology Research 7, n.º 1 (13 de marzo de 2017): 50. http://dx.doi.org/10.5539/jmbr.v7n1p50.
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Streptococcus sanguinis is a commensal and early colonizer of oral cavity as well as an opportunistic pathogen of infectious endocarditis. Extracting the soluble proteome of this bacterium provides deep insights about the physiological dynamic changes under different growth and stress conditions, thus defining “proteomic signatures” as targets for therapeutic intervention. In this protocol, we describe an experimentally verified approach to extract maximal cytoplasmic proteins from Streptococcus sanguinis SK36 strain. A combination of procedures was adopted that broke the thick cell wall barrier and minimized denaturation of the intracellular proteome, using optimized buffers and a sonication step. Extracted proteome was quantitated using Pierce BCA Protein Quantitation assay and protein bands were macroscopically assessed by Coomassie Blue staining. Finally, a high resolution detection of the extracted proteins was conducted through Synapt G2Si mass spectrometer, followed by label-free relative quantification via Progenesis QI. In conclusion, this pipeline for proteomic extraction and analysis of soluble proteins provides a fundamental tool in deciphering the biological complexity of Streptococcus sanguinis.
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Paik, Sehmi, Lauren Senty, Sankar Das, Jody C. Noe, Cindy L. Munro y Todd Kitten. "Identification of Virulence Determinants for Endocarditis in Streptococcus sanguinis by Signature-Tagged Mutagenesis". Infection and Immunity 73, n.º 9 (septiembre de 2005): 6064–74. http://dx.doi.org/10.1128/iai.73.9.6064-6074.2005.
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ABSTRACT Streptococcus sanguinis is a gram-positive, facultative anaerobe and a normal inhabitant of the human oral cavity. It is also one of the most common agents of infective endocarditis, a serious endovascular infection. To identify virulence factors for infective endocarditis, signature-tagged mutagenesis (STM) was applied to the SK36 strain of S. sanguinis, whose genome is being sequenced. STM allows the large-scale creation, in vivo screening, and recovery of a series of mutants with altered virulence. Screening of 800 mutants by STM identified 38 putative avirulent and 5 putative hypervirulent mutants. Subsequent molecular analysis of a subset of these mutants identified genes encoding undecaprenol kinase, homoserine kinase, anaerobic ribonucleotide reductase, adenylosuccinate lyase, and a hypothetical protein. Virulence reductions ranging from 2-to 150-fold were confirmed by competitive index assays. One putatively hypervirulent strain with a transposon insertion in an intergenic region was identified, though increased virulence was not confirmed in competitive index assays. All mutants grew comparably to SK36 in aerobic broth culture except for the homoserine kinase mutant. Growth of this mutant was restored by the addition of threonine to the medium. Mutants containing an insertion or in-frame deletion in the anaerobic ribonucleotide reductase gene failed to grow under strictly anaerobic conditions. The results suggest that housekeeping functions such as cell wall synthesis, amino acid and nucleic acid synthesis, and the ability to survive under anaerobic conditions are important virulence factors in S. sanguinis endocarditis.
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Evans, Karra, Victoria Stone, Lei Chen, Xiuchun Ge y Ping Xu. "Systematic study of genes influencing cellular chain length in Streptococcus sanguinis". Microbiology 160, n.º 2 (1 de febrero de 2014): 307–15. http://dx.doi.org/10.1099/mic.0.071688-0.
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Streptococcus sanguinis is a Gram-positive bacterium that is indigenous to the oral cavity. S. sanguinis, a primary colonizer of the oral cavity, serves as a tether for the attachment of other oral pathogens. The colonization of microbes on the tooth surface forms dental plaque, which can lead to the onset of periodontal disease. We examined a comprehensive mutant library to identify genes related to cellular chain length and morphology using phase-contrast microscopy. A number of hypothetical genes related to the cellular chain length were identified in this study. Genes related to the cellular chain length were analysed along with clusters of orthologous groups (COG) for gene functions. It was discovered that the highest proportion of COG functions related to cellular chain length was ‘cell division and chromosome separation’. However, different COG functions were also found to be related with altered cellular chain length. This suggested that different genes related with multiple mechanisms contribute to the cellular chain length in S. sanguinis SK36.
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Senty Turner, Lauren, Sankar Das, Taisei Kanamoto, Cindy L. Munro y Todd Kitten. "Development of genetic tools for in vivo virulence analysis of Streptococcus sanguinis". Microbiology 155, n.º 8 (1 de agosto de 2009): 2573–82. http://dx.doi.org/10.1099/mic.0.024513-0.
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Completion of the genome sequence of Streptococcus sanguinis SK36 necessitates tools for further characterization of this species. It is often desirable to insert antibiotic resistance markers and other exogenous genes into the chromosome; therefore, we sought to identify a chromosomal site for ectopic expression of foreign genes, and to verify that insertion into this site did not affect important cellular phenotypes. We designed three plasmid constructs for insertion of erm, aad9 or tetM resistance determinants into a genomic region encoding only a small (65 aa) hypothetical protein. To determine whether this insertion affected important cellular properties, SK36 and its erythromycin-resistant derivative, JFP36, were compared for: (i) growth in vitro, (ii) genetic competence, (iii) biofilm formation and (iv) virulence for endocarditis in the rabbit model of infective endocarditis (IE). The spectinomycin-resistant strain, JFP56, and tetracycline-resistant strain, JFP76, were also tested for virulence in vivo. Insertion of erm did not affect growth, competence or biofilm development of JFP36. Recovery of bacteria from heart valves of co-inoculated rabbits was similar to wild-type for JFP36, JFP56 and JFP76, indicating that IE virulence was not significantly affected. The capacity for mutant complementation in vivo was explored in an avirulent ssaB mutant background. Expression of ssaB from its predicted promoter in the target region restored IE virulence. Thus, the chromosomal site utilized is a good candidate for further manipulations of S. sanguinis. In addition, the resistant strains developed may be further applied as controls to facilitate screening for virulence factors in vivo.
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Moraes, Julianna J., Rafael N. Stipp, Erika N. Harth-Chu, Tarsila M. Camargo, José F. Höfling y Renata O. Mattos-Graner. "Two-Component System VicRK Regulates Functions Associated with Establishment of Streptococcus sanguinis in Biofilms". Infection and Immunity 82, n.º 12 (2 de septiembre de 2014): 4941–51. http://dx.doi.org/10.1128/iai.01850-14.
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ABSTRACTStreptococcus sanguinisis a commensal pioneer colonizer of teeth and an opportunistic pathogen of infectious endocarditis. The establishment ofS. sanguinisin host sites likely requires dynamic fitting of the cell wall in response to local stimuli. In this study, we investigated the two-component system (TCS) VicRK inS. sanguinis(VicRKSs), which regulates genes of cell wall biogenesis, biofilm formation, and virulence in opportunistic pathogens. AvicKknockout mutant obtained from strain SK36 (SKvic) showed slight reductions in aerobic growth and resistance to oxidative stress but an impaired ability to form biofilms, a phenotype restored in the complemented mutant. The biofilm-defective phenotype was associated with reduced amounts of extracellular DNA during aerobic growth, with reduced production of H2O2, a metabolic product associated with DNA release, and with inhibitory capacity ofS. sanguiniscompetitor species. No changes in autolysis or cell surface hydrophobicity were detected in SKvic. Reverse transcription-quantitative PCR (RT-qPCR), electrophoretic mobility shift assays (EMSA), and promoter sequence analyses revealed that VicR directly regulates genes encoding murein hydrolases (SSA_0094,cwdP, andgbpB) andspxB, which encodes pyruvate oxidase for H2O2production. Genes previously associated withspxBexpression (spxR,ccpA,ackA, andtpK) were not transcriptionally affected in SKvic. RT-qPCR analyses ofS. sanguinisbiofilm cells further showed upregulation of VicRK targets (spxB,gbpB, andSSA_0094) and other genes for biofilm formation (gtfPandcomE) compared to expression in planktonic cells. This study provides evidence that VicRKSsregulates functions crucial forS. sanguinisestablishment in biofilms and identifies novel VicRK targets potentially involved in hydrolytic activities of the cell wall required for these functions.
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Das, Sankar, Taisei Kanamoto, Xiuchun Ge, Ping Xu, Takeshi Unoki, Cindy L. Munro y Todd Kitten. "Contribution of Lipoproteins and Lipoprotein Processing to Endocarditis Virulence in Streptococcus sanguinis". Journal of Bacteriology 191, n.º 13 (24 de abril de 2009): 4166–79. http://dx.doi.org/10.1128/jb.01739-08.
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ABSTRACT Streptococcus sanguinis is an important cause of infective endocarditis. Previous studies have identified lipoproteins as virulence determinants in other streptococcal species. Using a bioinformatic approach, we identified 52 putative lipoprotein genes in S. sanguinis strain SK36 as well as genes encoding the lipoprotein-processing enzymes prolipoprotein diacylglyceryl transferase (lgt) and signal peptidase II (lspA). We employed a directed signature-tagged mutagenesis approach to systematically disrupt these genes and screen each mutant for the loss of virulence in an animal model of endocarditis. All mutants were viable. In competitive index assays, mutation of a putative phosphate transporter reduced in vivo competitiveness by 14-fold but also reduced in vitro viability by more than 20-fold. Mutations in lgt, lspA, or an uncharacterized lipoprotein gene reduced competitiveness by two- to threefold in the animal model and in broth culture. Mutation of ssaB, encoding a putative metal transporter, produced a similar effect in culture but reduced in vivo competiveness by >1,000-fold. [3H]palmitate labeling and Western blot analysis confirmed that the lgt mutant failed to acylate lipoproteins, that the lspA mutant had a general defect in lipoprotein cleavage, and that SsaB was processed differently in both mutants. These results indicate that the loss of a single lipoprotein, SsaB, dramatically reduces endocarditis virulence, whereas the loss of most other lipoproteins or of normal lipoprotein processing has no more than a minor effect on virulence.
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Li, Kewei, Alex H. Gifford, Thomas H. Hampton y George A. O’Toole. "Availability of Zinc Impacts Interactions between Streptococcus sanguinis and Pseudomonas aeruginosa in Coculture". Journal of Bacteriology 202, n.º 2 (4 de noviembre de 2019). http://dx.doi.org/10.1128/jb.00618-19.
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ABSTRACT Airway infections associated with cystic fibrosis (CF) are polymicrobial. We reported previously that clinical isolates of Pseudomonas aeruginosa promote the growth of a variety of streptococcal species. To explore the mechanistic basis of this interaction, we performed a genetic screen to identify mutants of Streptococcus sanginuis SK36 whose growth was no longer enhanced by P. aeruginosa PAO1. Mutations in the zinc uptake systems of S. sanguinis SK36 reduced growth of these strains by 1 to 3 logs compared to that of wild-type S. sanguinis SK36 when grown in coculture with P. aeruginosa PAO1, and exogenous zinc (0.1 to 10 μM) rescued the coculture defect of zinc uptake mutants of S. sanguinis SK36. Zinc uptake mutants of S. sanguinis SK36 had no obvious growth defect in monoculture. Consistent with competition for zinc driving coculture dynamics, S. sanguinis SK36 grown in coculture with P. aeruginosa showed increased expression of zinc uptake genes compared to that of S. sanguinis grown alone. Strains of P. aeruginosa PAO1 defective in zinc transport also supported ∼2-fold more growth by S. sanguinis compared to that in coculture with wild-type P. aeruginosa PAO1. An analysis of 118 CF sputum samples revealed that total zinc levels varied from ∼5 to 145 μM. At relatively low zinc levels, Pseudomonas and Streptococcus spp. were found in approximately equal abundance; at higher zinc levels, we observed a decline in relative abundance of Streptococcus spp., perhaps as a result of increasing zinc toxicity. Together, our data indicate that the relative abundances of these microbes in the CF airway may be impacted by zinc levels. IMPORTANCE Polymicrobial infections in CF cases likely impact patient health, but the mechanism(s) underlying such interactions is poorly understood. Here, we show using an in vitro model system that interactions between Pseudomonas and Streptococcus are modulated by zinc availability, and clinical data are consistent with this model. Together with previous studies, our work supports a role for metal homeostasis as a key factor driving microbial interactions.
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Zeng, Lin, Alejandro R. Walker, Kyulim Lee, Zachary A. Taylor y Robert A. Burne. "Spontaneous Mutants of Streptococcus sanguinis with Defects in the Glucose-PTS Show Enhanced Post-Exponential Phase Fitness". Journal of Bacteriology, 30 de agosto de 2021. http://dx.doi.org/10.1128/jb.00375-21.
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Genetic truncations in a gene encoding a putative glucose-PTS protein ( manL , EIIAB Man ) were identified in subpopulations of two separate laboratory stocks of Streptococcus sanguinis SK36; the mutants had reduced PTS activities on glucose and other monosaccharides. To understand the emergence of these mutants, we engineered deletion mutants of manL and showed that the ManL-deficient strain had improved bacterial viability in stationary phase and was better able to inhibit the growth of the dental caries pathogen Streptococcus mutans . Transcriptional analysis and biochemical assays suggested that the manL mutant underwent reprograming of central carbon metabolism that directed pyruvate away from production of lactate, increasing production of hydrogen peroxide (H 2 O 2 ) and excretion of pyruvate. Addition of pyruvate to the medium enhanced the survival of SK36 in overnight cultures. Meanwhile, elevated pyruvate levels were detected in the cultures of a small, but significant percentage (∼10%), of clinical isolates of oral commensal bacteria. Furthermore, the manL mutant showed higher expression of the arginine deiminase system than the wild type, which enhanced the ability of the mutant to raise environmental pH when arginine was present. To our surprise, significant discrepancies in genome sequence were identified between strain SK36 obtained from ATCC and the sequence deposited in GenBank. As the conditions that are likely associated with the emergence of spontaneous manL mutations, i.e. excess carbohydrates and low pH, are those associated with caries development, we propose that the glucose-PTS strongly influences commensal-pathogen interactions by altering the production of ammonia, pyruvate, and H 2 O 2 . Importance A health-associated dental microbiome provides a potent defense against pathogens and diseases. Streptococcus sanguinis is an abundant member of a health-associated oral flora that antagonizes pathogens by producing hydrogen peroxide. There is a need for a better understanding of the mechanisms that allow bacteria to survive carbohydrate-rich and acidic environments associated with the development of dental caries. We report the isolation and characterization of spontaneous mutants of S. sanguinis with impairment in glucose transport. The resultant reprograming of central metabolism in these mutants reduced the production of lactic acid and increased pyruvate accumulation; the latter enables these bacteria to better cope with hydrogen peroxide and low pH. The implications of these discoveries in the development of dental caries are discussed.
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Zhu, Bin, Xiuchun Ge, Victoria Stone, Xiangzhen Kong, Fadi El-Rami, Yan Liu, Todd Kitten y Ping Xu. "ciaR impacts biofilm formation by regulating an arginine biosynthesis pathway in Streptococcus sanguinis SK36". Scientific Reports 7, n.º 1 (diciembre de 2017). http://dx.doi.org/10.1038/s41598-017-17383-1.
Texto completoTesis sobre el tema "Streptococcus sanguinis SK36"
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Mahoney, Brian. "Examination of platelet adhesion by Streptococcus sanguinis". VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1978.
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Streptococcus sanguinis is a leading cause of infective endocarditis. Bacterial adhesion to platelets is likely important in the pathogenesis of infective endocarditis. Bacterial cell wall-anchored (Cwa) proteins may mediate this adhesion. To begin to test this hypothesis, S. sanguinis adhesion to platelets was examined in vitro. The requirement of 12 Cwa proteins for S. sanguinis-platelet adhesion was individually assessed, measuring adhesion of purified platelets to polystyrene wells coated with S. sanguinis strain SK36 or 12 isogenic Cwa protein mutants. Significantly fewer platelets adhered to wells coated with one mutant strain, VT1614. However, results of a whole-cell enzyme-linked immunosorbent assay (ELISA) showed that 8 mutants, including VT1614, adhered in significantly lower numbers to wells than did SK36. After accounting for unequal bacterial numbers, we determined there was no significant difference in platelet adhesion among the strains. This suggests that none of the Cwa proteins examined were required for S. sanguinis-platelet adhesion.
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Scott-Elliston, Ayana. "IN SEARCH OF A FUNCTION FOR AN UNCHARACTERIZED CONSERVED PROTEIN IN Streptococcus sanguinis SK36". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4889.
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With the number of fully sequenced bacterial genomes increasing in the past 7 years, it has been discovered that a large percentage of the putative protein coding genes have no known function. This lack of knowledge leaves scientists with an incomplete understanding of bacteria. In this study, conserved hypothetical protein mutants from Streptococcus sanguinis SK36 were screened on solid media with various environmental conditions. From these screens, the candidate protein, SSA_2372, displayed a sensitivity to acidic conditions. Its homolog in Bacillus subtilis 168, BSU00030, also displayed a sensitivity to pH conditions at its acid tolerance extremes unlike its other homolog in Escherichia coli, YbcJ. When the growth rate and cell yield was acquired, the sensitivity was shown to be significant for both SSA_2372 and BSU00030 mutants. Through data mining, it was determined that Firmicutes in this homolog family COG2501 may function as a regulator for recombination protein F.
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El-rami, Fadi. "A Systems Biology Approach For Predicting Essential Genes and Deciphering Their Dynamics Under Stress In Streptococcus sanguinis". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4925.
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Infectious diseases are the top leading cause of death worldwide. Identifying essential genes, genes indispensable for survival, has been proven indispensable in defining new therapeutic targets against pathogens, major elements of the minimal set genome to be harnessed in synthetic biology, and determinants of evolutionary relationships of phylogenetically distant species. Thus, essentiality studies promise valuable revenues that can decipher much of biological complexities.
Taking advantage of the available microbial sequences and the essentiality studies conducted in various microbial models, we proposed a framework for the prediction of essential genes based on our experimentally verified knowledge of the pathways involved in three essential xiv functions: genetic information processing, cell wall biosynthesis, and energy metabolism. We investigated physiological pathways in Kyoto Encyclopedia of Genes and Genomes (KEGG) database and developed a bioinformatics approach to predict essential genes in 13 different microbial species. Our in silico findings matched to a high degree the experimental data derived from essentiality studies conducted on the same microbial models, providing insights about the microbial lifestyles, including energy resources, cell wall structure, and ecological preferences, but not virulence tools and mechanisms.
Furthermore, we believe that essential genes have survived the evolutionary purifying selection due to their evolved capacity to re-wire genetic and protein networks in response to any emerging stress. In this sense, an environmental specificity (stress) provides a dominant determinant of an essential gene set. The new challenge was understanding the contribution of the essential genome in S. sanguinis to the coping mechanisms to different clinically relevant stress factors, namely temperature elevation (43oC) and sub-inhibitory concentration of ampicillin, an abundantly prescribed antibiotic for prophylaxis and treatment against S. sanguinis. The current project investigated the transcriptomic and proteomic profiles of essential genes and proteins, using RNA-seq and mass spectrometry respectively, under the impact of the two stressors separately, to elucidate the essential genome and proteome dynamics on a temporal basis and define “pathogenesis signatures” as potential therapeutic targets. We believe that the current findings will help characterize a bacterial model for studying the dynamics of essential genes and assist in designing evidence-based guidelines for drug prescription in clinical practice.
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Chiang, Yi Chien y 江宜蒨. "Characterization of the Type IV pili gene cluster Streptococcus sanguinis SK36". Thesis, 2011. http://ndltd.ncl.edu.tw/handle/88998232805241370382.
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碩士長庚大學
生物醫學研究所
99
Streptococcus sanguinis is a primary colonizer of human tooth and an opportunistic pathogen for subacute endocarditis. A Type IV pili (Tfp) gene cluster was reported in the complete genome of Streptococcus sanguinis SK36 recently. The goal of this research aimed to analyze the expression and function of this gene cluster. The Tfp gene cluster is composed of total 16 genes, from pilB to pilD. A contiguous transcript was detected between pilD and the downstream lytB by RT-PCR, suggesting that lytB is also part of the operon. Three transcription initiation sites, 153- (P1), 536- (P2) and 837-base (P3) 5’ to the translation start site of pilB, respectively, were detected by rapid amplification of cDNA ends (5’ RACE) analysis. Both the P2 and P3 mapped to a σ70-like promoters (5’-TTGACA-N17-TATACT), whereas only an extended -10 sequence was observed with the P1. An anti-PilA antibody was generated and used to examine the structure of the pil cluster encoded products by transmission electron microscopy (TEM). A short hair-like structure was observed in the wild-type SK36 but not the Pil-deficient mutant strain, indicating that pil cluster is responsible for the synthesis of this structure. Furthermore, the pil-deficient mutant strains exhibited reduced biofilm formation. However, neither the adherence to Hela cells nor the twitching motility was affected by the deletion in pil cluster. Taken together, these results suggest that the pil cluster is responsible for the synthesis of a surface structure, and this structure is associated with biofilm formation. The multiple transcription initiation sties with long 5’ untranslated regions suggested the presence of a complex regulation system for the expression of the pil cluster.
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Tseng, Tzu Ying y 曾姿穎. "Characterization and functional analysis of the type IV pili gene cluster in Streptococcus sanguinis SK36". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/33875483902144865967.
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碩士長庚大學
生物醫學研究所
101
Streptococcus sanguinis is a member of the dental plaque and occasionally causes infective endocarditis. Thus far the gene cluster (pil) encoding type IV pili (Tfp) was found only in the genome of Streptococcus sanguinis SK36. Previous studies by using 5’ RACE analysis revealed 3 putative transcription initiation sites 5’ to the pil cluster. Short hair-like structures were observed on the surface of SK36 by using anti-SSA_2315 (PilA) antiserum under transmission electron microscopy. However, the biological functions of the Tfp in S. sanguinis SK36 remains unknown. This study aims to analyze the expression and function of the pil cluster. By using various pil promoter-reporter fusion strains, it was found that all 3 promoters were functional. The activity of a transcriptional fusion containing all 3 promoters was higher in the ccpA-deficient host than that in the wild-type background, indicating that the expression of the pil operon is subject to the regulation of CcpA. Western analysis of the PilA protein indicated that the biogenesis of Tfp was regulated by growth phases, with the highest expression at the early stationary phase. Inactivation of SSA_2313-2315 led to a 40% reduction in adherence to HeLa cells and squamous cell carcinoma (SCC-4) compared to the wild-type strain. Taken together, the expression of the pil cluster was regulated by a complex system and the biosynthesis of Tfp was closely associated with the development of growth phase. The binding of S. sanguinis SK36 Tfp to host cells supports the role of Tfp in the pathogenesis of S. sanguinis SK36.
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Wu, Hui Yu y 吳蕙妤. "Regulation and functional analysis of the type IV pili gene cluster in Streptococcus sanguinis SK36". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/m9564z.
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