Which of the following statements about quorum sensing is incorrect? A. It is a mechanism of cell-to-cell communication B. Acyl homoserine lactones (AHLs) are used for signaling by Gram+ bacteria C. It is mechanism that allows bacteria to count themselves D. A model organism for the study of quorum sensing is the luminescent bacterium Vibrio fishe

Which of the following statements about quorum sensing is incorrect? A. It is a mechanism of cell-to-cell communication B. Acyl homoserine lactones (AHLs) are used for signaling by Gram+ bacteria C. It is mechanism that allows bacteria to count themselves D. A model organism for the study of quorum sensing is the luminescent bacterium Vibrio fishe

Concepts of Biology

1st Edition

ISBN:9781938168116

Author:Samantha Fowler, Rebecca Roush, James Wise

Publisher:Samantha Fowler, Rebecca Roush, James Wise

Chapter17: The Immune System And Disease

Section: Chapter Questions

Problem 15RQ: Autoantibodies are probably involved in ________. a. reactions to poison ivy b. pollen allergies c....

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Identify which of the following statements is a lie? Select one: a. Bacterial biofilms due to quorum sensing can be found on medical equipment and implants such as hip or knee replacements or heart pacemakers. b. Quorum sensing uses autoinducers as signaling molecules. Autoinducers are signaling molecules secreted by bacteria to communicate only with the same species of bacteria. c. The first evidence of bacterial communication was observed in a bacterium that has a symbiotic relationship with Hawaiian bobtail squid.
Gram negative cell walls contain lipopolysaccharide (LPS) as a unique component. All of the following apply to LPS EXCEPT O LPS is composed of mycolic acids that protect the cell from phagocytosis LPS is a PAMP that can be recognized by toll-like receptors (TLRS) as a foreign molecule fo rphagocytosis O LPS can be a target for specific IgG for ADCC-opsonization LPS can be recognized by B cells in the aosence of MHC molecules All of the answers apply, no exception O LPS is found in the outer membrane of Gram negative cells
In the light of the mechanisms of signal transduction pathways, DESCRIBE how:
G-protein-coupled receptors on phagocytes link microbe recognition with increased efficiency of intracellular killing. The NBT (Nitro Blue Tetrazolium) test is used to diagnose the genetic disorder Chronic Granulomatous Disease (CGD). To perform this test, peripheral blood cells from the patient are stimulated with bacterial extracts, and then incubated with the NBT compound. Normal neutrophils turn blue in this test due to cleavage of the compound, while patient neutrophils remain uncolored, as shown in Figure below. Name a neutrophil receptor that is likely to be stimulated by the bacterial extract in this assay, and describe how this receptor regulates the activity of the enzyme that cleaves NBT.
1. Construct one plot including the data for the WT and the MC4R mutants presenting the differences in membrane localisation. 2.Obtain approximate Emax and EC50 values from the graphs. 3.Why the ratio of PE/GFP fluorescence is measured in the FACS experiment, instead of measuring only total PE fluorescence? 4.Explain the effect that each mutation causes in the function of MC4R, and how they can be linked to disease.
A mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAG
The antimicrobial peptides (AMPs) are a special class of nonspecific cell-derived mediators with broad-spectrum antimicrobial properties. Choose the answers below that describe their activity. made in response to an invading pathogen damage cell membranes of invaders utilize antibodies engulf pathogen disrupt intracellular function of pathogen
Intercellular communication has been studied in detail in Myxococcus xanthus. Review the life cycle of this developmentally complex microbe and indicate at what points during this process intercellular signaling molecules might be exchanged and the message they would convey.
Which of the following small GTP-binding proteins does NOT play a role in cell migration during chemotaxis? O Cap Z Rho Cdc42 O All of the listed GTPases play a role in cell migration O Rac ◆ Previous
You have isolated a new species of infectious bacteria. The bacterium releases a toxin that you believe is adversely affecting heterotrimeric Gs (stimulatory)-protein-based signaling. To explore this hypothesis you use an epithelial cell line that is expressing a cyan fluorescent protein (CFP)-labeled α subunit and a yellow fluorescent protein (YFP)-labeled β subunit of a heterotrimeric Gs-protein. CFP emits blue light and has excitation and emission wavelengths of 440 nm and 490 nm, respectively. YFP emits yellow light and has excitation and emission wavelengths of 490 nm and 527 nm, respectively. To test your hypothesis, you perform two experiments. First, you apply a signaling ligand known to activate this Gs protein and track yellow fluorescence. Second, you apply the signaling ligand and the purified bacterial toxin simultaneously and track yellow fluorescence. Which of the following conclusion will you draw based on the above experimental data? The toxin locks the α subunit…
Would an antibody response against the B subunit protect against the effects of the toxin?
Quorum sensing controls the expression of virulencein many pathogenic bacteria. Usually, pathogens express toxins in response to receptor activation by ligand binding at high cell density. V. cholerae (thecausative agent of cholera) does the opposite; its virulence genes are expressed only at low cell densitybecause its quorum-sensing receptor is repressed byligand binding. The unusual “reversed” mechanismfor activating virulence genes in V. cholerae has suggested to scientists a simple idea for generating a newkind of antibiotic for the treatment of cholera.Explain