Short Answer Questions for Exam 2, Biology 250
  1. Of what subunits is DNA composed? Describe its general structure.
  2. If you exposed Serratia marcescens to ultraviolet light, it sometimes loses its ability to make an orange pigment. What two kinds of genetic changes could account for this? Define them.
  3. Distinguish between induced mutations and spontaneous mutations.
  4. Explain how a base analog like 5-bromuracil could cause a change in a base pair.
  5. Other chemicals, called alkylating agents, change the way an existing base pairs rather than replacing a base and then pairing differently. For example, EMS (ethyl methane sulfonate) causes G (guanine) to occasionally pair with A (adenine) instead of C (cytosine). Can you figure out how this could result in a changed base pair? How many generations will it take?
  6. How does ultraviolet radiation cause mutations?
  7. What happens when a mutation is lethal?
  8. Give 5 examples of nonlethal results of mutation.
  9. Contrast mutation and recombination as means of genetic change in bacteria.
  10. In recombination, what are the roles of the donor and recipient cells?
  11. In bacteria, what are three mechanisms of transfer of genetic information?
  12. For each of the mechanisms in the preceding question: Is cell contact required? What is transferred from one cell to the other? Is there some agent that assists the transfer? Does recombination always take place?
  13. What is recombinant DNA? Cloning a gene? Genetic engineering?
  14. Describe the process of making recombinant DNA for insulin:
    1. How do you get the piece of human chromosome that contains the desired gene?
    2. What do you need to isolate from a bacterium (E. coli)?
    3. What do you do to it to make the next step possible?
    4. What has to happen next to make a recombinant plasmid?
    5. What enzymes have you used so far? To do what?
    6. Now that you have a recombinant plasmid, by what mechanism will you get it back into E. coli?
    7. If you want E. coli to produce a large quantity of the desired product (insulin), what will you do next?
    8. If you want a large number of copies of the gene for insulin, what will you do next?
  15. Discuss the application of recombinant DNA to the treatment of disease (gene therapy). How does it work in the example we discussed in class? (severe combined immunodeficiency, due to ADA deficiency)
  16. Give several examples of substances that can be or have been prepared by genetic engineering.
  17. Why are antibiotics that target cell walls and protein synthesis more likely to be clinically useful than those that target cell membranes and nucleic acid synthesis?
  18. Make a table of the antibiotics/drugs mentioned in class, correlating each antibiotic/drug with its mode of action and/or target of action in cells.
  19. Discuss antibiotic resistance: how organisms become resistant to an antibiotic and possible strategies for decreasing the incidence of antibiotic resistance.
  20. Define infection, disease, host, normal flora, pathogen, virulence and opportunistic pathogen.
  21. In the interaction between host and pathogen, what happens when the host's defenses overwhelm the pathogen?
  22. What happens when the pathogen's invasive strategies establish it in the host in spite of the host's defenses?
  23. What happens when the host's defenses and the survival strategies of the pathogen are evenly balanced??
  24. What kinds of tissue injury can result in initiating inflammation?
  25. What are the classic symptoms of inflammation?
  26. Make sure you know the sequence of events in an inflammatory reaction. Can you tell it to someone as if it were a story?
  27. The initiating event for the early steps in inflammation is mast cell degranulation. What is released from the mast cell granules that causes these immediate effects on capillaries?
  28. What is the significance of diapedesis in the inflammatory reaction?
  29. Describe the process of phagocytosis. Name two kinds of cells that are phagocytes. What happens to the material that is phagocytized in each kind of cell?
  30. How is the damaged tissue restored to normal (if possible)?
  31. What distinctions can you make between inflammatory reactions and immune responses?