Download ALE 7 - Biol 100

Answer Key
Biology 100
Instructor: K. Marr
ALE #9. DNA Structure and DNA Replication Practice Problems
DNA Structure
1. a. What is a nucleotide? Why are nucleotides important, that is, what do your cells use them for?
Nucleotides are important since they are the building blocks (i.e. monomers) from
which the nucleic acids DNA and RNA are made. Each nucleotide consists of three
parts linked together by covalent bonds: a phosphate, sugar and a nitrogen base.
More specifically, the phosphate is linked to the #5 carbon of the sugar (deoxyribose
in DNA, ribose in RNA) and nitrogen containing base is connected to the #1 carbon of
the sugar.
b.
Label the three main components (phosphate, sugar, nitrogen base) and the 5’ and 3’ ends of the simplified
representation of a nucleotide below.
c.
There are four different nucleotides in DNA. What makes each of these nucleotides different?
Each DNA nucleotide differs by which of the four bases it contains: adenine, thymine,
guanine or cytosine.
d.
There are four different nucleotides in RNA. What makes each of these nucleotides different?
Each RNA nucleotide differs by which of the four bases it contains: adenine, Uracil,
guanine or cytosine.
e.
Indicate the nitrogen bases found in DNA and RNA by completing the table below.
Nitrogen Bases Found in DNA
Nitrogen Bases found in RNA
Adenine
Thymine
Guanine
Cytosine
Adenine
Uracil
Guanine
Cytosine
DNA Replication
2. a. Why is it DNA replication necessary for all organisms on earth today?
DNA replication is essential for all living things since DNA is the genetic material that
contains all the information needed to guide the life processes. Hence, for any species to
survive, it must replicate its DNA before cellular division so that each of the daughter
cells contains all the genetic information needed for life.
b. When during the cell cycle does DNA replication occur?
During the S-phase of the cell cycle
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3.
DNA Replication. Use the hypothetical representation of a double stranded DNA molecule, below, to complete the
following tasks.
a. Complete the base sequence of the complementary strand of the hypothetical DNA molecule diagrammed below.
b. Label the 5’ and 3’ ends of each strand.
c. Use dashed lines to indicate hydrogen bonding between paired bases.
d. Show how this molecule would be replicated:
o Draw the molecule partially ―unzipped‖ while undergoing replication, followed by the resulting daughter
molecules with their correct nucleotide sequences and base pairing.
o Use two colors, one for the template (or parent) strands, and another for the newly synthesized daughter
strands.
4. Once Watson and Crick determined the structure of DNA, they had a very good hunch about how DNA replicated itself.
How does DNA structure account for the ability of DNA to replicate itself?
Since weak hydrogen bonds connect the two strands of a DNA molecule, Watson and Crick
reasoned, the first step in DNA replication would involve the separation of the two strands.
This would allow, they postulated, complementary nucleotides to pair with each of the two
separated strands, according to the base pairing rules, A to T, and G to C. The net result is
the formation of two double stranded DNA molecules, each identical in base sequence to the
original parent molecule.
5.
Central Dogma of Biology. How does DNA structure account for the ability of genes to control a phenotype (i.e. a
particular physical or behavioral feature of an organism)?
DNA  mRNA  Protein  Controls phenotype
In short, DNA encodes a specific mRNA, which encodes a specific protein, which does a
specific job in the body, thereby controlling the phenotype. The genes that are active in any
particular cell is determined by environmental factors during development (i.e. cellular
differentiation) and after development (e.g. UV light stimulates the activity of genes involved
in melanin production to protect skin cells from UV light)
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In more detail, the nucleotide base sequence in DNA controls the kind of proteins a cell can
make: The base sequence in DNA determines the base sequence in a specific mRNA, which in
turn controls the order of amino acids in a specific protein. It’s the order of amino acids in a
protein that determines its shape, and its shape controls its function. It’s proteins in cells that
control the phenotype: some proteins are structural (e.g. hair, nails, and muscle fibers),
others act as enzymes. Enzymes determine which chemical processes will occur within cells,
thereby controlling the phenotype of an organism (e.g. control chemical processes such as the
production of eye, hair, and skin pigments).
6.
a.
Name the enzyme responsible for lengthening each strand during DNA replication by repeatedly adding
nucleotides to the 3’ end of each strand.
DNA polymerase
b.
How does this enzyme “know” which nucleotide to use during DNA replication—that is, what “rules does the
enzyme follow.
DNA polymerase follows the base pairing rules: A (adenine) to T (thymine) and G
(guanine) to C (cytosine)
c.
Name the enzyme that proofreads and corrects any errors it finds in the DNA strands after the completion of DNA
replication.
DNA polymerase
d.
What is a mutation? Why do they occur?
A mutation is any change in the base sequence in DNA. Mutations can lead to a change in
the amino acid sequence in a protein, which can change the function of a protein, and
hence a change in the phenotype, or they can be silent—that is, change the codon in
mRNA, but only to one that codes for the same amino acid.
Mutations are caused by mutagens—e.g. UV light, X-Rays, chemicals that attach to
nucleotide bases in DNA (e.g. chemicals in cigarette smoke). Mutagens cause DNA
polymerase to make mistakes during DNA replication. If mistakes are not caught and
corrected during proof-reading—also performed by DNA polymerase—then mutations
are the result. There are three major kinds of mutations: nucleotide deletions, insertions
and substitutions.
e.
During which phase of the cell cycle do mutations occur?
S-phase
Relating DNA Replication to the Cell Cycle
7. a. As in mitosis, the chromosomes are duplicated prior to the start of meiosis I. How many duplicated chromosomes
will there be in a human “pregamete” cell just before the start of meiosis I?
46 duplicated chromosomes (i.e. 46 two-chromatid chromosomes)
b.
How many DNA molecules are in a human “pre-gamete” cell just before the start of meiosis I?
c.
Just after meiosis II and cytokinesis (the division of the cytoplasm) how many chromosomes are there in each
gamete?
d.
Just after meiosis II and cytokinesis how many DNA molecules are there?
92 DNA molecules (2 molecules of DNA per duplicated chromosome)
23 unduplicated chromosomes (i.e. 23 one-chromatid chromosomes)
23 DNA molecules (1 molecule of DNA per chromosome)
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8.
Diploid “pregamete” cells from a hypothetical mammal were examined under a microscope and found to contain 4
chromosomes.
a.
Draw one of these cells in metaphase I of meiosis.
Consider the size and shape of your
chromosomes.
b.
A drug is given to this animal so that the S phase (DNA
replication) does not occur. Draw one of these cells in
metaphase I of meiosis. Draw your chromosomes so
that the size and shape is consistent with the cell you
drew in part a.
Applying your knowledge
9. a. Diagram the way in which two guanine nucleotides would join together to form a single strand of DNA two
nucleotides long. Use the guanine nucleotide drawn below as the first nucleotide (nucleotide #1, below), and draw
another guanine nucleotide in the space to the right of the label ―Nucleotide #2.‖
 Label the sugar, base, and phosphate portions of the first nucleotide.
 Number the carbons in the sugar of the first nucleotide.
 Label the 5’ and 3’ ends of this mini DNA molecule
 Be sure to connect the two nucleotides together in the appropriate places by a covalent bond—see figures
11.5 and 11.8 in Essentials of Biology by Mader 2nd ed if you need help understanding how to connect
nucleotides.
b.
AZT (Azido thymidine) is a drug currently used to treat AIDS patients. AZT is similar to the thymine nucleotide
(i.e. the ―T‖ nucleotide found in all DNA). AZT differs from the T nucleotide in that an ―azido‖ chemical group is
attached to its sugar. Now add an AZT (Azido thymidine) nucleotide (shown below) to the growing strand in the
diagram above. Connect the AZT nucleotide by a covalent bond to the guanine nucleotide above it.
c. Explain why AZT prevents another nucleotide from being added to the growing DNA strand and then explain how
AZT will affect DNA replication.
The “Azido” group attached to the # 3 carbon of AZT nucleotide blocks the next nucleotide from
being added to an elongating strand of DNA during DNA replication, effectively inhibiting DNA
replication. When HIV infects a cell its RNA is “reverse transcribed” by reverse transcriptase to
produce DNA. AZT blocks this process, thus inhibiting HIV reproduction.
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10. Most nerve cells do not replicate their DNA upon reaching maturity. Suppose that a cell biologist measured the amount
of DNA in several different types of human cells:
1) Nerve cells
2) Sperm cells
3) Bone cells just starting interphase
4) Skin cells in the S phase
5) Intestinal cells just beginning mitosis
She found x amount of DNA in the nerve cells. Use this fact and the information in the table below to identify
Cells A - D. Note: If the cell cycle and mitosis are a bit rusty, review Section 8.2 in Essentials of Biology by Mader .
Cell Type
Nerve Cell
Cell A
Amount of DNA in Cell
x
2x
Cell B
1.6x
Cell C
0.5x
Cell D
x
Identity of Cell
Nerve Cell
#5 = Intestinal cells just beginning mitosis
#4 = Skin cells in the S-phase
#2 = Sperm cells
#3 = Bone cells
11. Over-exposure to ultra violet light from the sun or cancer beds (i.e. tanning beds!) may cause a person’s skin to burn
and eventually peel. What is the biological/genetic cause/reasons why burnt skin peels? What are the biological
advantages and disadvantages of peeling? Your response should include a discussion of DNA repair enzymes,
apoptosis, and the p53 gene.
UV light can severely damage DNA—break the sugar-phosphate backbone and causing adjacent
thymine bases within one strand to react with each other to form a thymine dimmer. Minor damage
to DNA can be repaired by various DNA repair enzymes such as DNA polymerase. If the DNA is
severely damaged (as is the case when you get a sunburn), the damaged DNA activates the p53 gene,
a gene that initiates cell suicide, also known as apoptosis. This is what causes the skin to peel. The
primary advantage of the skin peeling is ridding the body of cells with damaged DNA, thus
preventing cells with mutant DNA from reproducing—this could lead to cancer. Unfortunately, only
the skin cells with severely damaged DNA are lost. Left behind are cells with DNA that is less
damaged. If the damage is not caught and repaired, then reproduction of these cells will lead to cells
with mutations, mutations that could lead to cancer.
Something you may find interesting......
The number of times a cell is capable of dividing is called the Hayflick limit—named after Leonard Hayflick, the biologist
that discovered it in 1961. It’s intriguing to note that the cells of longer-lived species of animals have a larger Hayflick limit
(e.g. Human fibroblast cells have a Hayflick limit of 40-60, the long-lived Galapagos Tortoise (lifespan >> 150 years) has a
Hayflick limit of about 110), while those of short -lived species have smaller Hayflick limit (e.g. mice live 2-3 years and
have a Hayflick limit of about 10-15). The Hayflick limit appears to be related to the length of the telomeres associated with
that species. Although cells continue living when they reach the Hayflick limit, they often become senescent. Senescent cells
are dedifferentiated (i.e. do not perform the functions they were originally programmed to do), appear structurally abnormal
under the microscope, and gradually lose their ability to function properly. On the other hand, many cells cease to divide
after they are formed (e.g. most neurons in the brain), yet they do not normally become senescent. Although the exact
relationship between the Hayflick limit and longevity is still unclear, it is a hot area of current research.
12. What are telomeres and why are they essential for the survival of our species and all other eukaryotic species?
Telomeres are repeated DNA sequences [(TTAGGG)n in humans] found at the ends chromosomes
that protect the ends of the chromosome from shortening. At birth, telomeres consist of repeated
TTAGGG DNA sequences, which become shorter each time a cell replicates its DNA. Since telomeres
do not contain genes, the shortening of telomeres protects genes from becoming damaged. Hence
telomeres act as protective a cap that protects genes from getting damaged each time a cell divides—
without telomeres cell division would destroy genes, a recipe for extinction of a species .
Every time a replicates its DNA base pairs off the ends of the telomeres. When the telomeres reach
a critical length (usually after 40 to 60 divisions in human cells) a cell senesces (or ages) and stops
dividing. Senescent cells become dedifferentiated, stop performing their normal functions and secrete
substances that gradually injure neighboring cells. Telomere shortening has been suggested to be a
"clock" that regulates how many times an individual cell can divide.
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13. Most somatic cells (i.e. body cells) in the human body can divide about 40-60 times before they ultimately stop
dividing. On the other hand, cancer cells, stem cells (undifferentiated cells that divide to give rise to other cell types;
e.g. stem cells in the bone marrow give rise to the various types of blood cells, including RBC’s and WBC’s), and the
germ stem cells (those that produce the gametes—egg and sperm cells) are not limited in the number of times they can
divide. Explain why stem cells and cancerous cells have unlimited reproductive capability, while somatic cells can
divide only a finite number of times. What roles do the telomerase gene and the enzyme telomerase play?
Stem cells and cancer cells have unlimited reproductive capacity since the telomerase gene is
active in these cells. The telomerase gene codes for the enzyme telomerase, an enzyme that
rebuilds the telomeres each time a cell replicates its DNA, thereby preventing telomere
shortening. The telomerase gene is not active in somatic cells; hence their telomeres shorten
each time DNA is replicated, thus leading to cellular senescence.
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