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Bio 321 Exam 3
Due 10/31/01
Name ________________________
Please answer 6 of the following questions
1. Shigella flexneri is a gram-negative enteric pathogen that exhibits a cell biology of infection virtually
identical to Listeria monocytogenes. S. flexneri mediates actin based motility by binding to WASP, a protein
that mediates actin polymerization in immune cells. How might binding WASP promote bacterial movement?
Based on this information, one might propose that the virulence of Shigella flexneri could be reduced by
disrupting actin polymerization. However, a human disease called Wiskott Aldrich Syndrome results from a
mutation in WASP. The disease renders patients more susceptible to infectious disease due to a defect in
WASP-mediated actin polymerization in immune cells. Why do you suppose that patients with Wiskott
Aldrich Syndrome are more susceptible to infectious disease?
2. Briefly describe the invasion assay using to study Yersinia invasion. How was the Yersinia invasion protein
(Invasin) discovered? Bonus: Fibronectin is the natural ligand for the Invasin receptor. Invasin coated beads
are internalized while fibronectin-coated beads are not. Provide a hypothesis to explain this observation.
3. The following statements refer to the Yersiniae. Identify which statements are true and which are false and
briefly explain each answer.
A. Demonstrate a number of temperature-dependent characteristics
B. Are exclusively extracellular pathogens
C. Share a common virulence plasmid
D. Show calcium-dependent growth
4. Listeria monocytogenes with in-frame deletion mutations within the actA gene are able to enter the host
cytosol normally but fail to nucleate actin and are consequently avirulent and fail to form a plaque in tissue
culture cells. Complementation of this mutant with ActA on a plasmid results in bacteria that nucleate actin,
but are still avirulent and fail to form plaques. Provide a possible explanation for the lack of complementation
of virulence. Propose an experiment to test your hypothesis.
5. Explain why Pseudomonas aeruginosa is described as a true opportunistic pathogen. What features present
in other pathogens might make P. aeruginosa capable of causing infection in healthy people?
6. How would you attempt to prove or disprove the importance of non-pilus adhesins in Pseudomonas
aeruginosa pathogenesis? Discuss a potential model systems you would use and the advantages or
disadvantages of that system.
7. What is quorum sensing and how is it used to regulate gene expression in P. aeruginosa? Describe the
autoinducer molecule and the role it plays in quorum sensing.