Solution Manual for Biology 1st

Edition by Brooker Widmaier

Graham and Stiling
Full download at link: https://testbankpack.com/p/solution-
manual-for-biology-1st-edition-by-brooker-widmaier-
graham-and-stiling-isbn-978007326807-0073268070/

Chapter 14
Mutation, DNA Repair, and Cancer

Instructional Strategies and Activities

• This chapter provides a number of opportunities to point out the elegant

nature of the genetic code. An excellent example is in the discussion of gene
mutations and how the degenerate or redundant property of the genetic code
drastically reduces the impact of these mutations on the proteome.

• A good technique to help students keep the different types of mutations

straight in their minds is to construct a chart in class with either the name or
the description of the mutation filled in. Ask for responses for filling in the
missing information. If you want to challenge your students and find out if
they really understand the material well, you can present unlabeled figures of
the different types of mutations (such as the DNA and amino acid sequences
from Table 14.1) and ask the students what type of mutation is depicted.

• The same techniques can be used for the mechanisms of DNA repair.
Hypothetical examples of DNA damage could be presented, and students
would choose the appropriate repair mechanism. This could also be turned
into a group activity linking mutation types and repair mechanisms. In the first
“round” of the activity, each group of students would generate an original and
a modified (mutated) DNA sequence similar to those presented in Table 14.1.
For the second “round” groups would exchange DNA sequences, and would
then have to suggest which repair mechanism would fix the damage, and
what the resulting repaired DNA sequence would look like.

• You might wish to ask your students whether or not they think DNA repair
mechanisms might have any disadvantages. If they understand mutations,

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 they should be able to tell you that DNA repair could hypothetically reduce the
number of adaptations in a population. You could follow this up by then
asking why, if there is a potential disadvantage, DNA repair mechanisms are
so ubiquitous and varied. Your students should be able to tell you that this is
likely because the vast majority of mutations are not beneficial, so the benefit
of having DNA repair mechanisms is probably much greater than the potential
cost. Discussions of this type typically do not take very long, and help
students to truly understand the nature and importance of mutations and
repair mechanisms.

Student Misconceptions

• Students often have many misconceptions about mutations. A common one

is that all mutations are harmful. Students should understand that while the
majority of mutations are harmful or at best neutral, adaptations also arise
from mutations. This fact is mentioned in the text, but is often overlooked by

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 students, especially if they focus on mutations being the result of damage to
DNA.

• The idea that DNA repairs itself is likely to be new to many of your students.
They often do not realize that in most organisms the majority of damage to
DNA is repaired, and that observed mutation rates would be orders of
magnitude higher if not for repair systems.

• Students often have a number of misconceptions about cancer. One of which

is that cancer can be contagious, like a cold. Interestingly enough, some
types of cancer (such as cervical cancer) could be considered to be
contagious because they are caused by viruses that can be transmitted from
one individual to another. Therefore, the idea that cancer is only transmitted
from person to person through heredity is also a misconception.

• Remind students that only mutations that occur in gametes can be passed to
offspring. The mutations that occur in somatic cells will not affect the next
generation.

Beyond the Book

• Model organisms such as the fruit fly, Drosophila, have short generation times
which allow researchers to follow mutations down family lines. Drosophila
can go from egg to adult in around seven to ten days, depending on
incubation temperature. Bacterial generation times are even quicker with
some bacteria reproducing via binary fission every 20 minutes.

• A study published in 2000 in the journal Genetics reports that the mutation
rate in humans could be 175 per diploid genome per generation, and that the
rate of mutations in males could be 4 times higher than the rate in females.
The full text of the article can be found at:
http://www.genetics.org/cgi/content/full/156/1/297

• Antioxidants such as vitamins A, C, and E and the mineral selenium are

famous for their ability to help reduce the risk of cancer. Antioxidants directly
or indirectly react with free radicals that can result in DNA damage and
mutations resulting in activation of proto oncogenes. The efficacy of
antioxidants in humans remains uncertain. Much (but not all) of the
reputation of antioxidants regarding cancer prevention has been based on a
famous study conducted in China in 1993 (J Natl Cancer Inst 85:1483-91), as
well as a number of small-scale cell culture and rodent studies. However, a
number of other studies have shown either no effect of antioxidants or even
an increased risk of cancer (e.g., New England Journal of Medicine 330:1029-
35, Cancer Research 54(7 Suppl):2038s–43s). Clearly, more research needs
to be done to clarify the role of antioxidants in prevention of cancer, but until
then, we should eat as much dark chocolate as possible, just in case!

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• According to the American Cancer Society, the number of cancer deaths in
the United States in 2003 was approximately 500 times greater than in 1930.
Of course, as we have pointed out to students in other chapters, the increase
in the number of cancer deaths may not be due to an actual increase in the
incidence of cancer. Possible explanations include an increased mutation
rate due to internal or external factors, but the increased cancer mortality may
also be due to better cancer detection methods allowing for more deaths to
be attributed to cancer. Cancer incidence rates vary by sex and race. For
example, African Americans have the highest incidence of cancer, while
American Indians and Alaskan Natives have the lowest. The statistics
compiled by the ACS can be found at:
http://www.cancer.org/docroot/stt/stt_0.asp

Additional Web Resources

• Milestones in Genetics: Timeline – An interactive timeline which is a

downloadable program file from the Human Genome Project.
http://www.genome.gov/Pages/EducationKit/download.html

• Talking Glossary of Genetic Terms – A website provided by the Human

Genome project in which many genetic terms are defined with the layperson
in mind.
http://www.genome.gov/glossary.cfm

• American Cancer Society – The homepage for the ACS provides a wealth of
information about cancer and treatment.
http://www.cancer.org/docroot/home/index.asp

• Gene Reviews – A collection of articles concerning heritable diseases,

including diseases attributed to genetic mutations, such as the BRAC1 and
BRAC2 breast cancer mutation.
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gene

• Genes and Disease – A discussion of genetic diseases in humans including

the underlying mutation that causes the disease.
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gnd

• DNA From The Beginning: Mutations are changes in genetic information –

This website offers an animation illustrating Muller’s work with fruit flies, a
problem set, Muller’s biography and web links.
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gnd

• Blazing a Genetic Trail – A website from the Howard Hughes Medical Center
that discusses many aspects of genetic diseases, such as mutations which

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 give rise to diseases, inheritance of the diseases, and searches for cures for
diseases.
http://www.hhmi.org/genetictrail/d100.html

• Inherited Diseases – An activity from the Koshland Science Museum that

allows the user to search for the mutation that causes hemochromatosis.
http://www.koshlandsciencemuseum.org/exhibitdna/inh05activity.jsp

Etymology of Key Terms

apoptosis programmed cell death (from the Greek apo- away from and
piptein- to fall)

benign not cancerous (from the Latin bene- well and gignere- to beget)

-carcin tumor, cancer (from the Greek karkinos- ulcerous sore, cancer)

chimeric a female monster composed of many animal parts: a lion’s head, a

goat’s body and a snake’s tail (from the Greek chimaria- female
goat)

-gen that which produces (from the Greek genes- born or produced)

germ beget (from the Latin gignere- to beget)

malignant invasive cancer cells (from the late Latin malignant-)

metastatic cancer cells capable of moving to other parts of the body (from the
Greek meta- change and histanai- to set )

neutro- neutral; having no charge or affiliation (from the Latin neuter-

neither)

onco- tumor (from the Greek onkos- bulk)

proto- first (from the Greek protos- first)

sarcoma connective tissue tumor (from the Greek sarkoun- to grow flesh)

somat- the body of an organism (from the Greek soma- body)

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