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- do not copy from cheggRESEARCH ARTICLE TITLE: "On the rapidity of antibiotic resistance evolution facilitated by a concentration gradient" Full Article Reseach: Hermsen, R., Deris, J. B., & Hwa, T. (2012). On the rapidity of antibiotic resistance evolution facilitated by a concentration gradient. Proceedings of the National Academy of Sciences, 109(27), 10775–10780. doi:10.1073/pnas.1117716109 QUESTION: 1. In biological/science manner, what are your comments on how the authors constructed their ARTICLE/RESEACH TITLE (see article).Results from a Kirby Bauer antibiotic assay on a Gram-negative bacterial culture are described as follows: A) the bacterium is resistant to penicillin, an antibiotic that targets synthesis of the peptidoglycan cell wall and B) the bacterium is resistant to tetracycline, an antibiotic that targets the small subunit of the ribosome, inhibiting protein synthesis. Which of the results represents intrinsic resistant and which represents acquired resistants?
- Describe the viable but non culturable (VBNC) dormant state and the production of small colony variants (SCVs) type of dormant state. Differentiate these two surviving strategies of bacteria in harsh environments from spore-forming strategic survival of extremophiles.Various antimicrobial drugs to treat microbial infection have diverse mechanism of action. Consider the following antimicrobial drugs: A. Seconeolitsine, known as DNA topoisomerase I inhibitor in bacteria. (i) Explain briefly how inhibiting DNA topoisomerase I is a good mechanism of action for an antibiotic, include possible molecular machineries being targeted. (ii) What would be an appropriate response if seconeolitsine works well by stating the state of supercoiling in bacteria. (iii) To prove your answer (ii), you test the condition of bacterial DNA by running gel electrophoresis, one has been treated with seconeolitsine (+ sample) and the other one is not (- sample). Explain the position of each + sample and – sample band on the gel in reference to the point of origin (where you load your samples) or how far each DNA sample travel across agarose gel. (iv) Explain why you would expect answer (iii) for each + sample and – sample. B.…Before JCVI-syn3.0 was produced, what steps were used to create a synthetic Mycoplasma cell? Put the events below into the correct order. Drag and drop the events into the proper sequence from left to right. ▸ View Available Hint(s) First Step Transformed cells are detected by the presence of lacz, which causes them to cleave Xgal and produce a blue color. Yeast is transformed using Mycoplasma mycoides fragments. The synthetic chromosome is transformed into Mycoplasma capricolum. The synthetic Mycoplasma mycoides chromosome is purified. DNA fragments assemble through homologous recombination in yeast. Reset Help Last Step
- 1.(a) Explain in detail the different modes of horizontal gene transfer in acquiring antibiotic resistance genes in bacteria. 1.(b) Explain briefly the differences in bioenergetics between a cyanobacterium and Ralstonia eutrophaDiscuss some advantages and disadvantages of bacteriophage therapyin treating bacterial infections."On the rapidity of antibiotic resistance evolution facilitated by a concentration gradient" ABSTRACT The rapid emergence of bacterial strains resistant to multiple antibiotics is posing a growing public health risk. The mechanisms underlying the rapid evolution of drug resistance are, however, poorly understood. The heterogeneity of the environments in which bacteria encounter antibiotic drugs could play an important role. E.g., in the highly compartmentalized human body, drug levels can vary substantially between different organs and tissues. It has been proposed that this could facilitate the selection of resistance mutants, and recent experiments support this. To study the role of spatial heterogeneity in the evolution of drug resistance, we present a quantitative model describing an environment subdivided into relatively isolated compartments with various antibiotic concentrations, in which bacteria evolve under the stochastic processes of proliferation, migration, mutation and…
- "On the rapidity of antibiotic resistance evolution facilitated by a concentration gradient" ABSTRACT The rapid emergence of bacterial strains resistant to multiple antibiotics is posing a growing public health risk. The mechanisms underlying the rapid evolution of drug resistance are, however, poorly understood. The heterogeneity of the environments in which bacteria encounter antibiotic drugs could play an important role. E.g., in the highly compartmentalized human body, drug levels can vary substantially between different organs and tissues. It has been proposed that this could facilitate the selection of resistance mutants, and recent experiments support this. To study the role of spatial heterogeneity in the evolution of drug resistance, we present a quantitative model describing an environment subdivided into relatively isolated compartments with various antibiotic concentrations, in which bacteria evolve under the stochastic processes of proliferation, migration, mutation and…One of the early results shows that the post-centrifugation pellet of encapsulated cells also contains EA1 and/or Sap. Why is this not proof that Bacillus anthracis cells have both an S-layer and a capsule simultaneously? I need help finding the answer in the article and explain in short answer link to article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106848/One of the early results shows that the post-centrifugation pellet of encapsulated cells also contains EA1 and/or Sap. Why is this not proof that Bacillus anthracis cells have both an S-layer and a capsule simultaneously? I need help finding the answer in the article and explain in short answer link to article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106848/