Genetics: From Genes to Genomes, 5th edition
Genetics: From Genes to Genomes, 5th edition
5th Edition
ISBN: 9780073525310
Author: Leland H. Hartwell, Michael L. Goldberg, Janice A. Fischer, Leroy Hood, Charles F. Aquadro
Publisher: McGraw-Hill Education
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Chapter 15, Problem 38P

Quorum sensing controls the expression of virulence in many pathogenic bacteria. Usually, pathogens express toxins in response to receptor activation by ligand binding at high cell density. V. cholerae (the causative agent of cholera) does the opposite; its virulence genes are expressed only at low cell density because its quorum-sensing receptor is repressed by ligand binding. The unusual “reversed” mechanism for activating virulence genes in V. cholerae has suggested to scientists a simple idea for generating a new kind of antibiotic for the treatment of cholera. Explain?

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In a set of experiments, T cells from wild-type (WT) or bm12 mice were mixed in vitro with antigen-presenting cells (APCs), in the presence or absence of the superantigen staphylococcal enterotoxin B (SEB), and T cell proliferation was measured. The data from these experiments are shown in the figure below. What is the explanation for the results in Rows 1–4 of the table?. Why does the T cell response to SEB (Rows 5–8) show a different pattern than the response to bovine insulin? Note: Epitope mapping studies identified amino acid residues 1–14 of the bovine insulin A chain as the peptide recognized by CD4 T cells from wild-type mice.
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Genetics: From Genes to Genomes, 5th edition

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