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Transcript
Chapter Objectives: Chapters 18~19: Genetics of Viruses and Bacteria
1. Describe the contributions of A. Mayer, D. Ivanowsky, M. Beijerinck, and W.
Stanley to the discovery of viruses
2. List and describe the structural components of viruses
3. Explain why viruses are obligate parasites
4. Describe 3 patterns of viral genome replication
5. Explain the role of reverse transcriptase in retroviruses
6. Describe how viruses recognize host cells
7. Distinguish between lytic and lysogenic reproductive cycles using phage T 4
and phage λ as examples.
8. Outline the procedure for measuring phage concentration in a liquid medium
9. Describe several defenses bacteria have against phage infection
10. Using viruses with envelopes and RNA viruses as examples, describe
variations in replication cycles of animal viruses
11. Explain how viruses may cause disease symptoms and describe some medical
weapons used to fight viral infections
12. List some viruses that have been implicated in human cancers and explain
how tumor viruses transform cells
13. Distinguish between horizontal and veritcal routes of viral transmission in
plants
14. List some characteristics that viruses share with living organisms and
explain why viruses do not fit our usual definition of life
15. Provide evidence that viruses probably evolved from fragments of cellular
nucleic acid
16. Describe the structure of a bacterial chromosome
17. Describe the process of binary fission in bacteria and explain why replication
of the bacterial chromosome is considered to be semiconservative
18. List and describe the 3 natural processes of genetic recomgination in
bacteria
19. Distinguish between general transduction and specialized transduction
20. Explain how the F plasmid controls conjugation in bacteria
21. Explain how bacterial conjugation differs from sexual reporduction in
eukaryotic organisms
22. For donor and recipient bacterial cells, predict the consequences of
conjugation between the following
a. F+ and F - cell
b. HFr and F - cell
23. Define transposon and describe 2 essential types of nucleotide sequences
found in transposon DNA
24. Distinguish between an inseretion sequence and a complex transposon
25. Describe the role of transponases and DNA polymerase in the process of
transposition
26. Explain how transposons can generate genetic diversity
27. Briefly describe the 2 main strategies cells use to control metabolism
28. Explain why grouping genes into an operan can be advantageiojs
29. using the trp operon as an example, explain the concept of an operon and the
functionof the operator, repressor, and corepressor
30. Distinguish between structural and regulatory genes
31. Describe how th lac operon functions and explain the role of the inducer
allolactose
32. Explain how repressible and inducible enzymes differ and how these
differences reflect differences in the pathwyas they control
33. Distinguish between positive and negative control and give examples of each
from the lac operon
34. Expalin how CAP is affect glucose concentration
35. Describe how E. coli uses the negative and positive controls of the lac operon
to economize on RNA and protein synthesis
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52.
Compare the organization of prokaryotic and eukaryotic genomes
Describe the current model for progressive levels of DNA packing
Explain how histones influence folding in eukaryotic DNA
Distinguish between heterochromatin and euchromatin
Using the Barr body as an example, describe the function of
heterochromatin in interphase cells
Describe where satellite DNA is found and what role it may play in the cell
Describe the role of telomeres in solving the end-replication problem with
thelagging DNA strand
Using the genes for rRNA as an example, explain how multigene families of
identical genes can be advantageous for a cell
Using α-globin and β-globin genes as examples, describe how multigene
families of nonidentical genes probably evolve, including the role of
transposition
Explain the potential role that pormoters and enhancers play in
transcriptional control
Explain why the nuclear envelope in eukaryotes offers a level of posttrascriptional control beyond that found in prokaryotes
Explain why the ability to rapidly degrade mRNA can be an adaptive
advantage for prokaryotes
Describe the importance of mRNA degradation in eukaryotes and describe
how it can be prevented
Explain how gene expression may be controlled at the translational and posttranslational level
Compare the arrangement of coordinately controlled genes in prokaryotes
and eukaryotes
Explain how eukaryotic genes can be coorinately expressed and give some
examples of coorinate gene expression eukaryotes
Provide evidence from studies of polygene chromosomes that eukaryotic
gene expression is controlled at transcription and that gene regulation
repsonds to chemical signals such as steroid hormones
53. Describe the key steps of steroid hormone action on gene expression in
vertebrates
54. In general terms, explain how genome plasticity can influence gene
expression
55. Describe the effects of gene amplification, selective gene loss, and DNA
methylation
56. Explain how rearrangements in the genome can activate or inactivate genes
57. Explain the genetic basis for antibody diversity
58. Explain how DNA methylation may be a cellular mechanism for long-term
control of gene expression andhow it can influence early development
59. Describe the normal control mechanisms that can convert proto-oncogenes
to oncogenes
60. Explain how changes in tumor-suppressor genes can be involved int
ransforming normal cells into cancerous cells
61. Explain how oncogenes are involved in virus-induced cancers
Chapter Terms:
Chapter 18 Terms
capsid
reverse transcriptase
F factor
viral envelope
HIV
episome
bacteriophage (phage)
AIDS
F plasmid
host range
vaccine
R plasmid
lytic cycle
virion
transposon insertion
sequence
virulent virus
prion
lysogenic cycle
nucleoid
temperate virus
transformation
prophage
transduction
provirus
conjugation
operator
operon
repressor
regulatory gene
corepressor
retrovirus
inducer
Chapter 19 Terms
histones
gene amplification
activator
nucleosome
retrotransposons
DNA-binding domain
heterochromatin
immunoglobulins
alternative splilcing
euchromatin
differentiation
proteasomes
repetitive DNA
DNA methylation
oncogenes
satellite DNA
genomic imprinting
proto-oncogenes
Alu elements
histone acetylation
tumor-suppressor genes
multigene family
control elements
ras gene
pseudogene
enhancers
p53 gene
Chapter Outline Framework
A. The Genetics of Viruses
1. Researchers discovered viruses by studying a plant disease
2. A virus is a genome enclosed in a protective coat
3. Viruses can reproduce only within a host cell
4. Phages reproduce using lytic or lysogenic cycles
5. Animal viruses are diverse in their modes of infection and replication
6. Plant viruse are serious agricultural pests
7. Viruses may have evolved from other mobile genetic elements
B. The Genetics of Bacteria
1. The short generation span of bacteria facilitates their evolutionary
adaptation to changing environments
2. Genetic recombination produces new bacterial strains
3. The control of gene expression enables individual bacteria to adjust their
metabolism to environmental change
C. The Structure of Chromatin
1. Chromatin structure is based on successive levels of DNA packing
D. Genome Organization at the DNA Level
1. Repetitive DNA and othe noncoding sequences account for much of a
eukaryotic genome
2. Gene families have evolved by duplication of ancestral genes
3. gene amplification, loss, or rearrangement can alter a cell's genome
E. The Control of Gene Expression
1. Each cell of a multicellular eukaryote expresses only a small fraction of its
genome
2. The control fo gene expression can occur at any step in the pathway from
gene to functional protein
3. Chromatin modifications affect the availability of genes for transcription
4. Transcription initiation is controlled by proteins that interact with DNA and
with each other
5. Post-transcriptional mechanisms play supporting roles in the control fo gene
expression
F. The Molecular Biology of Cancer
1. Cancer results from genetic changes that affect the cell cycle
2. Oncogene proteins and faulty tumor-suppressor proteins
3. Multiple mutations underlie the development of cancer