Overview of the regulatory networks in expression of group A streptococcal virulence genes. +, positive regulation; —, negative regulation. Overview of.

Slides:



Advertisements
Similar presentations
PowerPoint Presentation Materials to accompany
Advertisements

Gene regulation. Gene expression models  Prokaryotes and Eukaryotes employ common and different methods of gene regulation  Prokaryotic models 1. Trp.
Copyright © 2005 Brooks/Cole — Thomson Learning Biology, Seventh Edition Solomon Berg Martin Chapter 13 Gene Regulation.
CHAPTER 8 Metabolic Respiration Overview of Regulation Most genes encode proteins, and most proteins are enzymes. The expression of such a gene can be.
Advanced Microbial Physiology Lecture 3 Sigma Factors.
Microbial Genetics (Micr340) Lecture 15 Regulation of Gene Expression.
Gene Control in Eukaryotes In eukaryotic cells, the ability to express biologically active proteins comes under regulation at several points: 1. Chromatin.
Test system for systems biology Four distinct types of global datasets were generated and analyzed 1.Proteome analysis quantitative proteomics (ICAT technology)
Molecular Basis for Relationship between Genotype and Phenotype DNA RNA protein genotype function organism phenotype DNA sequence amino acid sequence transcription.
Regulation of Gene Expression Chromosomal Map begins at OriC; units of minutes. –Only structural genes for enzymes are shown here. –Their control regions.
Gene Regulation In 1961, Francois Jacob and Jacques Monod proposed the operon model for the control of gene expression in bacteria. An operon consists.
Controls over Genes.
Chapter 10-How Protein are Made Section 1-From Genes to Proteins – Traits are determined by proteins, that are built by DNA. – Proteins are NOT built by.
12.4 Mutations Changes in the genetic material Mistake in copying, carcinogens Single gene = gene mutation Entire chromosome = chromosomal mutation.
Gene Expression: Prokaryotes and Eukaryotes AP Biology Ch 18.
BIOL 2416 Chapter 17: Bacterial Operons
Chapter 8, part B Microbial Genetics.
Chapter 8, part B Microbial Genetics.
Transcription(I) 王之仰.
Control of Gene Expression in Prokaryotes
Alignment table: group 4
Which of the following would be the corresponding amino acid sequence that would be translated as a protein product of the following segment of DNA? A.
Background for Molecular Biology of Lactase Persistence
OPERONS * Indicated slides borrowed from: Kim Foglia
Prediction of Regulatory Elements for Non-Model Organisms Rachita Sharma, Patricia.
Control of Gene Expression
Molecular Mechanisms of Gene Regulation
OUTLINE 3 Control of Gene Expression in Prokaryotes
Regulation of Gene Expression
Regulation of Gene Expression
Relationship between Genotype and Phenotype
Gen Expression Constitutive Enzymes not Regulated
Metabolic Pathways and Additional Levels of Regulation: Attenuation
Relationship between Genotype and Phenotype
Regulation of Gene Expression
Regulation of Transcription Initiation
Control of Gene Expression in Eukaryotic cells
The Small RNA IstR Inhibits Synthesis of an SOS-Induced Toxic Peptide
Regulation of Gene Expression
Mapping Global Histone Acetylation Patterns to Gene Expression
Regulation of S. enterica SPI-1 and LEE of EPEC. (A) SPI-1 of S
Nat. Rev. Nephrol. doi: /nrneph
Transcriptional Regulation in Prokaryotes.
Gene Regulation in Prokaryotes
Volume 89, Issue 7, Pages (June 1997)
Regulatory RNAs in Bacteria
RND efflux operons in P. aeruginosa.
Objective 3: TSWBAT recognize the processes by which bacteria respond to environmental changes by regulating transcription.
MexT-associated downregulation of oprD expression.
Prokaryotic (Bacterial) Gene Regulation
Gene arrangement in the B
Coregulation of mexEF-oprN and oprD in P. aeruginosa.
Examples of PAI of various pathogens.
Chapter 8, part B Microbial Genetics.
Diagram of the group A streptococcal cell covered with an outer hyaluronic acid capsule and the group A carbohydrate, consisting of a polymer of rhamnose.
Structure of PrfA (A) and its target DNA sequences in PrfA-regulated promoters (B). Structure of PrfA (A) and its target DNA sequences in PrfA-regulated.
The arsenal of virulence factors expressed by GAS to thwart the host innate immune response. The arsenal of virulence factors expressed by GAS to thwart.
Relationship between Genotype and Phenotype
Schematic representing the activation of the complement cascade.
Regulation of expression of the AcrAB-TolC efflux system of E. coli.
The mexR and nalC mutations decrease C-30 inhibition of P
Membrane-associated proteins expressed by human epithelial cells that function as receptors for Afa/Dr adhesins. Membrane-associated proteins expressed.
Cross talk between the virulence elements.
Proposed mechanisms of Ag presentation.
Pathogenesis of oncogenic HPV
The Alp family of proteins.
Comparison of the van gene clusters.
Cartoon illustrating the genomic organization of a typical mucosal high-risk HPV. The genome contains early and late regions, which relate to the positions.
Microarray transcriptional heat map analysis of cell wall stimulon activation of hVISA/VISA (defined by population analysis and vancomycin broth MIC) relative.
Overview of some general cell wall characteristics of VSSA and VISA strains showing the key regulatory elements linked to intermediate-level vancomycin.
Presentation transcript:

Overview of the regulatory networks in expression of group A streptococcal virulence genes. +, positive regulation; —, negative regulation. Overview of the regulatory networks in expression of group A streptococcal virulence genes. +, positive regulation; —, negative regulation. Short dashed lines indicate CovR regulation, and long dashed lines represent regulation by Mga. Solid lines show the correlation between growth phase (exponential [light lines] or stationary [darker lines]). As shown in the figure, Mga activates transcription of several genes, including those for M protein (emm), C5a peptidase (scpA), M-like proteins (mrp, enn, and fcR), serum opacity factor (sof), and secreted inhibitor of complement (sic) (95, 101, 355, 358, 422). Mga feeds back to positively regulate itself and functions as a 62-kDa protein to bind to the promotor region of genes that it regulates (417). The genes involved in the mga regulon are shown in Table 3, and an overview of regulation is shown in the diagram above. A global negative regulator of mga was identified in a few strains and called nra. In addition to repressing Mga synthesis 4- to 16-fold, nra was a negative regulator ofprtF2, the gene for the fibronectin-binding protein F2, and the collagen-binding protein gene (cpa) in group A streptococci. The Nra protein sequence was 62% homologous to RofA, a positive transcriptional regulator of the fibronectin-binding protein (prtF) and itself in response to increased oxygen levels (426). RofA and Mga may influence the expression of genes involved in adhesion in different environments (426).csrR and csrS or covR andcovS are a pair of genetic loci in group A streptococci that encode a two-component regulatory system (327). Inactivation of csrR or covR resulted in a striking increase in transcription of the capsule synthesis genes of the hasoperon and a corresponding increase in hyaluronic acid capsule production (327). Subsequent work confirmed these observations and demonstrated binding of the CsrR protein to the promoter region upstream of the has operon (42). The CsrR or CovR protein acts as a transcriptional regulator. Production of a nonpolar mutation in csrR or covRincreased transcription of several other virulence genes, includingska (streptokinase), sagA (streptolysin O), andspeF (mitogenic factor) but had no effect on mga,emm, scpA, speB, or speC. Thus, the CovR or CsrR response regulator repressed transcription of several virulence operons in group A streptococci (172). Since multiple unrelated genes were controlled by csrR, an alternative nomenclature was given to the csrR-csrS locus,covR-covS for control of virulence genes. ThecsrR-csrS or covR-covS sensor-regulator gene pair represent a new regulatory pathway affecting expression of several group A streptococcal virulence genes which are not regulated bymga and has been found in all group A streptococcal strains tested (172). (Reprinted from reference172 with permission from the publisher.)‏ Madeleine W. Cunningham Clin. Microbiol. Rev. 2000; doi:10.1128/CMR.13.3.470