BIOL 238 Review 2009: Difference between revisions

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This page provides review questions for [http://biology.kenyon.edu/courses/biol238/biol238syl09.html BIOL 238] (Spring 2009).  Answers may be posted by students.
This page provides review questions for [http://biology.kenyon.edu/courses/biol238/biol238syl10.html BIOL 238] (Spring 2010).  Answers may be posted by students.
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==Chapter 1==
<br><br>
[Note: To answer a question in edit mode, please place your answer like this, inbetween two double-line breaks.]
<br><br>
<b>1. What historical discoveries in microbiology, both medical and environmental, laid the foundation for the discovery by Rita Colwell and Anwar Huq of an inexpensive way for Bangladeshi villagers to prevent cholera?</b>
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<b>2. The Colwell interview depicts three different ways of visualizing microbes.  What are the capabilities and limitations of each method?  Which method(s) would have been available before Leeuwenhoek?  By Leeuwenhoek?  For Peter Mitchell and Jennifer Moyle?</b>
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<b>3. Compare the "family tree" of life as drawn by Herbert Copeland, Robert Whittaker, Lynn Margulis, and Carl Woese.  How were they similar, and how did they differ?  How did their differences relate to different tools available for study?</b>
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<b>4. Outline the different contributions to medical microbiology and immunnology of Louis Pasteur, Robert Koch, and Florence Nightingale.  What methods and assumptions did they have in common, and how did they differ?</b>
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<b>5. Does the human immune system react similarly to both attenuated pathogens and more active pathogens?</b>
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<b>6. Outline the different contributions to environmental microbiology of Sergei Winogradsky and Martinus Beijerinck.  Why did it take longer for the significance of environmental microbiology to be recognized, as compared with pure-culture microbiology?</b>
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<b>7. It is always necessary to prepare a tissue culture to study viruses, as they can't grow without a host cell. Do certain bacteria need tissue in their cultures?</b>
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<b>8. How did Alexander Fleming's cultured plate of <i>Staphylococcus</i> become moldy with <i>Penicillium notatum</i>? Is it common for petri dishes to become moldy if left in the open air for too long?</b>
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==Chapter 2==
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<br>
<b>1. Explain what features of bacteria you can study by: light microscopy; fluorescence microscopy; scanning EM; transmission EM.</b>
==Chapter 7==
<br>
<b>1. What are the relative advantages and limitations of bidirectional replication versus rolling circle replication?  What kind of genetic entities are likely to favor one over the other?</b>
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<br><br>
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<b>2. Explain the difference between detection and resolution.  Explain how resolution is increased by magnification; why can't the details be resolved by your unaided eye?  Explain why magnification reaches a limit; why can it not go on resolving greater detail?</b>
<b>2. What kinds of mutant phenotypes reveal aspect of the mechanism of DNA replication and cell division?  Explain two specific examples.</b>
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<br><br>
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<b>3. How does refraction enable magnification?</b>
<b>3. Explain how it's possible for the replisome to replicate the leading and lagging strands simultaneously.</b>
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<br><br>
<br><br>
<b>4. Explain why artifacts appear, even with the best lenses. Explain how you can tell the difference between an optical artifact and an actual feature of an image.</b>
<b>4. During resolution of a catenane, how might a major mutation occur affecting the entire genome? How do you think this mutation is prevented?</b>
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<br><br>
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<b>5. How can "detection without resolution" be useful in microscopy?  Explain specific examples of dark-field observation, and of fluorescence microscopy.</b>
<b>5. During rapid growth, why would a bacterial cell die if the antibiotic drug “forms a physical barrier in front of the DNA replication complex.”?</b>
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<br><br>
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<b>6. Explain how the Gram stain works.  What are its capabilities and limitations?  How does the Gram stain relate to bacterial phylogeny?</b>
<b>6. What are the relative advantages and limitations of bidirectional versus rolling-circle replication of DNAExplain in terms of different genome sizes, types, and cell situation when replication occurs.</b>
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<br><br>
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<b>7. If shapes of bacteria are common to many taxonomic groups, including spirochetes which cause Lyme disease as well as others, how accurately can different bacteria be identified just based on shape?</b>
<b>7. When you sequence a genome, how do you know where the base pairs in the genome are located since the DNA used to sequence the genome is in fragments?</b>
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<br><br>
<b>8. Why should we believe scanning probe microscopy (SPM) is accurate? If scientists should be concerned by possible artifacts in EM why wouldn‘t they be concerned about artifacts or even further complications in SPM?</b>
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<br><br>
==Chapter 8==
<b>9. When would you use TEM over SEM, or vice versa?</b>
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==Chapter 3==
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<br>
<b>1. For one of your card pathogens, explain the type of cell membrane, cell wall, and outer membrane if any.  Explain how any particular components of the membrane and envelope contribute to pathogenesis.</b>
<b>1. Explain how a biochemical experiment can demonstrate the specific protein targeted by a new antibiotic that impairs transcription.</b>
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<br><br>
<br><br>
<b>2. Compare and contrast the structure and functions of the cell and the S-layer.</b>
<b>2. If <i>Mycoplasma genitalium</i> cannot synthesize its own amino acids, does it have extensive/multiple protein channels (ABC pumps) to let amino acids pass its membrane? If proteins are made of amino acids, though, how did the first M. genitalium’s protein channels come into existence? </b>
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<b>3. The antibiotic linezolid prevents the 50S ribosome subunit from binding the 30S subunit. If you isolate ribosomes by ultracentrifugation, how might the results in the tube look different with linezolid present?</b>
<b>3. In tRNA, there are "unusual" bases not found in mRNA  How are these bases generated? Do you think they arise from a recently-evolved aspect of tRNA, or do you think they are an ancient phenomenon of the original RNA world? Explain.</b>
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<b>4. In the laboratory, what selective pressure may cause loss of S-layers over several generations of subculturingSimilarly, why would subcultured bacteria lose flagella?</b>
<b>4. What kinds of pharmaceutical agents could you design to act on gene promotersExplain using protein and/or RNA molecules.</b>
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<br><br>
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<b>5. For one of your card pathogens, explain what specialized structures it has, such as pili or storage granules.  Explain how they might contribute to pathogenesis.</b>
<b>5. Why do you think bacterial cells absorb protein and nucleic acids that are exported by other bacteria?</b>
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<br><br>
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<b>6. Why might a human cell have a protein complex that imports a bacterial toxin?  How might such a situation evolve?</b>
<b>6. How could you sequence the genome of an unculturable microbe?</b>
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<b>7. What aspects of the outer membrane prevent phagocytosis, and how?</b>
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<br><br>
==Chapter 9 and 10==
<b>8. If the peptidoglycan cell wall is a single molecule, how does the cell expand and come apart to form two daughter cells?</b>
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<b>9. Explain two different ways that an aquatic phototroph might remain close to the light, or that an aerobe might remain close to the air surface.</b>
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==Chapter 4==
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<br>
<b>1. Suppose in Yellowstone Park, Mammoth Spring, a thermophilic bacterium (<i>Bacillus steareothermophilus</i> increases its population size by ten-fold in 40 minutes.  What is the generation time, or doubling timeWhy might these bacteria grow faster than <i>Bacillus megaterium, in our laboratory at Kenyon?</i></b>
<b>1. In the process of conjugation, how are genes moved? Are genes moved individually or in groupsCould part of a gene be moved? </b>
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<b>2. <i>Mycobacterium tuberculosis</i>, the cause of tuberculosis (TB), has a generation time of 18 hours.  How many days will it take to grow a colony containing a million cells?  What is the consequence for research on TB?</b>
<b>2. How are microbial species defined?  What is the role of vertical phylogeny; and the role of horizontal gene exchange? Explain why species definition is a problem.</b>
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<b>3. Explain the different mechanisms that membrane protein complexes can use to transport nutrients: ABC transporters, group translocation, and ion cotransport (symport and antiport).  Discuss the advantages and limitations of each mechanism.</b>
<b>3. Why is competence factor exported out of the cell to bind to ComD externally in transformation of Streptococcus? Why doesn't the molecule bind internally? Doesn't exporting CF waste energy? </b>
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<b>4. Under what growth conditions do bacteria eat the contents of other bacteria?  How do they manage do do this?  What is the significance for medical research?</b>
<b>4. If a spontaneous mutation occurs to form an apurinic site, transcription and replication are hindered, but what actually happens when the replisome gets to the hole where the base should be? </b>
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<b>5. In the laboratory, why is it important to grow isolated coloniesWhat can occur in colonies that we might not notice?  What research problems cannot be addressed with isolated colonies?</b>
<b>5. Explain how a DNA sequence inverts during phase variation.  Would you expect it to revert at the same rateWhy or why not?</b>
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<br><br>
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<b>6. Compare and contrast the advantages and limitations of different responses to starvation: stationary phase; sporulation; and fruiting body formation.</b>
<b>6. Explain the different propagation strategies available to a replicative transposon. What are various ways the transposon could spread within a cell? Among organisms?</b>
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<b>7. Explain how the <i>ara</i> operon works, and how it differs from the lac operon.</b>
==Chapter 5==
<br>
<b>1. Look through a grocery store, inspecting the labels of packaged foods.  What chemical preservatives do you recognize, and what is their mechanism for killing bacteria or inhibiting growth?  For example, propionate and sorbate are membrane-permeant acids that depress cytoplasmic pH.</b>
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<br><br>
<b>2. Explain the major difference between the effects of general sterilization and disinfectants, versus antibiotics such as penicillin or streptomycin.  Why do antibiotics rapidly select for resistant strains, whereas disinfectants and sterilizing agents do not?</b>
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<b>3. Explain which extreme environmental conditions select for membrane unsaturation.  What is the advantage of unsaturated membranes for these conditions?</b>
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<b>4. Explain how protein structure is modified during evolutionary adaptation to high temperatures, or to high pressure.</b>
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<b>5. Suppose it takes a heat treatment 3 minutes to halve the population of bacteria in the food.  How long will it take to decrease the bacteria content by 2D-values? Would you want to eat the food at this point?  Explain.</b>
<b>8. Explain how different mechanisms acting at different levels on DNA and RNA can modulate gene expression over a range of time scales, from multiple generations to within a few seconds.</b>
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<b>6. What kind of habitats will show halophiles?  What is the difference between moderate halophiles, extreme halophiles, and halotolerant organisms?  Describe what will happen to halophile populations in a pool under the hot sun.</b>
<b>9. Explain the roles of thermodynamic and kinetic effects in attenuation control of the <i>trp</i> operon.</b>
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<b>7. What is the mechanism of killing of organisms by ionizing radiation?  Why is ionizing radiation less effective on frozen foods?</b>
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==Wozniak lecture on Biofilms==
<br><br>
==Chapters 6 and 11==
<br>
<br>
<b>1. Discuss the different functions of different structural proteins of a virion, such as capsid, nucleocapsid, tegument and envelope proteins. How do these functions compare and contrast with functions of cellular proteins?</b>
<b>1. What do bacterial biofilms have in common with multicellular organisms? How do they differ?</b>
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<b>2. Explain how viruses are cultured, and how a pure isolate of a virus can be obtained.  How do the procedures differ from that of pure culturing bacteria?  What special difficulty arises when defining genetically pure isolates of RNA viruses such as herpes and HIV?</b>
<b>2. What are the advantages to bacteria of biofilm formation?  What properties do biofilms confer?</b>
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<b>3. How can strongly oncogenic viruses be assayed in culture, if they don't produce plaques?</b>
<b>3. Where in the body do biofilms form infections?  Why?</b>
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<b>4. What are the relative advantages of the virulent phage life cycle of phage T4; the lysis-lysogeny options of phage lambda; and the slow-release life cycle of phage M13? Under what conditions might each strategy be favored over the others?</b>
<b>4. Explain the basis of "twitching motility."  Compare and contrast twitching with flagellar motility. How does twitching motility promote biofilm development?</b>
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<b>5. Compare and contrast the life cycles of Herpes virus and HIV (AIDS). What do they have in common, and how do they differ?</b>
<b>5. How does the ara promoter work (pBAD)? How was pBAD used to test the role of the <i>psl</i> operon in bioflim development?</b>
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<br><br>
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<b>6. RNA viruses and DNA viruses represent fundamentally different reproductive strategies.  What are the relative advantages and limitations of each?  How do their different strategies impact the immune response, and the development of antiviral agents?</b>
<b>6. How was it proved that <i>psl</i> encodes PSL polysaccharide?  How does PSL compare in structure with alginate?</b>
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<br><br>


<br><br>
<b>7. Discuss the role of host-modulating viral proteins in in herpes viruses.  What various kinds of functions do these proteins serve for the virus; and what are their effects on the host?</b>
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<br><br>

Revision as of 15:47, 18 February 2010

This page provides review questions for BIOL 238 (Spring 2010). Answers may be posted by students.

Chapter 7


1. What are the relative advantages and limitations of bidirectional replication versus rolling circle replication? What kind of genetic entities are likely to favor one over the other?



2. What kinds of mutant phenotypes reveal aspect of the mechanism of DNA replication and cell division? Explain two specific examples.



3. Explain how it's possible for the replisome to replicate the leading and lagging strands simultaneously.



4. During resolution of a catenane, how might a major mutation occur affecting the entire genome? How do you think this mutation is prevented?



5. During rapid growth, why would a bacterial cell die if the antibiotic drug “forms a physical barrier in front of the DNA replication complex.”?



6. What are the relative advantages and limitations of bidirectional versus rolling-circle replication of DNA? Explain in terms of different genome sizes, types, and cell situation when replication occurs.



7. When you sequence a genome, how do you know where the base pairs in the genome are located since the DNA used to sequence the genome is in fragments?



Chapter 8


1. Explain how a biochemical experiment can demonstrate the specific protein targeted by a new antibiotic that impairs transcription.



2. If Mycoplasma genitalium cannot synthesize its own amino acids, does it have extensive/multiple protein channels (ABC pumps) to let amino acids pass its membrane? If proteins are made of amino acids, though, how did the first M. genitalium’s protein channels come into existence?



3. In tRNA, there are "unusual" bases not found in mRNA How are these bases generated? Do you think they arise from a recently-evolved aspect of tRNA, or do you think they are an ancient phenomenon of the original RNA world? Explain.



4. What kinds of pharmaceutical agents could you design to act on gene promoters? Explain using protein and/or RNA molecules.



5. Why do you think bacterial cells absorb protein and nucleic acids that are exported by other bacteria?



6. How could you sequence the genome of an unculturable microbe?



Chapter 9 and 10


1. In the process of conjugation, how are genes moved? Are genes moved individually or in groups? Could part of a gene be moved?



2. How are microbial species defined? What is the role of vertical phylogeny; and the role of horizontal gene exchange? Explain why species definition is a problem.



3. Why is competence factor exported out of the cell to bind to ComD externally in transformation of Streptococcus? Why doesn't the molecule bind internally? Doesn't exporting CF waste energy?



4. If a spontaneous mutation occurs to form an apurinic site, transcription and replication are hindered, but what actually happens when the replisome gets to the hole where the base should be?



5. Explain how a DNA sequence inverts during phase variation. Would you expect it to revert at the same rate? Why or why not?



6. Explain the different propagation strategies available to a replicative transposon. What are various ways the transposon could spread within a cell? Among organisms?



7. Explain how the ara operon works, and how it differs from the lac operon.



8. Explain how different mechanisms acting at different levels on DNA and RNA can modulate gene expression over a range of time scales, from multiple generations to within a few seconds.



9. Explain the roles of thermodynamic and kinetic effects in attenuation control of the trp operon.



Wozniak lecture on Biofilms


1. What do bacterial biofilms have in common with multicellular organisms? How do they differ?



2. What are the advantages to bacteria of biofilm formation? What properties do biofilms confer?



3. Where in the body do biofilms form infections? Why?



4. Explain the basis of "twitching motility." Compare and contrast twitching with flagellar motility. How does twitching motility promote biofilm development?



5. How does the ara promoter work (pBAD)? How was pBAD used to test the role of the psl operon in bioflim development?



6. How was it proved that psl encodes PSL polysaccharide? How does PSL compare in structure with alginate?