Molecular Biology of the Cell by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter by by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morg

CHAPTER 7 END-OF-CHAPTER PROBLEMS
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of different genes; some represent modified forms of a protein
that migrate to different positions. Pick out a couple
of sets of spots that could represent proteins that differ by
the number of phosphates they carry. Explain the basis for
your selection.
7–6 Comparisons of the patterns of mRNA levels
across different human cell types show that the level of
expression of almost every active gene is different. The
patterns of mRNA abundance are so characteristic of cell
type that they can be used to determine the tissue of origin
of cancer cells, even though the cells may have metastasized
to different parts of the body. By definition, however,
cancer cells are different from their noncancerous precursor
cells. How do you suppose then that patterns of mRNA
expression might be used to determine the tissue source of
a human cancer?
7–7 What are the two fundamental components of a
genetic switch?
7–8 The nucleus of a eukaryotic cell is much larger
than a bacterium, and it contains much more DNA. As a
consequence, a transcription regulator in a eukaryotic cell
must be able to select its specific binding site from among
many more unrelated sequences than does a transcription
regulator in a bacterium. Does this present any special
problems for eukaryotic gene regulation?
Consider the following situation. Assume that the
eukaryotic nucleus and the bacterial cell each have a single
copy of the same DNA binding site. In addition, assume
that the nucleus is 500 times the volume of the bacterium,
and has 500 times as much DNA. If the concentration of the
transcription regulator that binds the site were the same
in the nucleus and in the bacterium, would the regulator
occupy its binding site equally as well in the eukaryotic
nucleus as it does in the bacterium? Explain your answer.
7–9 Some transcription regulators bind to DNA and
cause the double helix to bend at a sharp angle. Such
“bending proteins” can affect the initiation of transcription
without directly contacting any other protein. Can you
devise a plausible explanation for how such proteins might
work to modulate transcription? Draw a diagram that illustrates
your explanation.
7–10 How is it that protein–protein interactions that
are too weak to cause proteins to assemble in solution
can nevertheless allow the same proteins to assemble into
complexes on DNA?
7–11 Imagine the two situations shown in Figure Q7–2.
In cell 1, a transient signal induces the synthesis of protein
A, which is a transcription activator that turns on
many genes including its own. In cell 2, a transient signal
induces the synthesis of protein R, which is a transcription
repressor that turns off many genes including its own. In
which, if either, of these situations will the descendants of
the original cell “remember” that the progenitor cell had
experienced the transient signal? Explain your reasoning.
(A) CELL 1
OFF
A
transcription
activator
(B) CELL 2
OFF
R
transcription
repressor
A
transient
signal
A
turns on transcription
of activator mRNA
R
transient
signal
R
turns on transcription
of repressor mRNA
Figure Q7–2 Gene regulatory circuits and cell memory (Problem 7–11).
(A) Induction of synthesis of transcription activator A by a transient
signal. (B) Induction of synthesis of transcription repressor R by a
transient signal.
7–12 Examine the two pedigrees shown in Figure Q7–3.
One results from deletion of a maternally imprinted autosomal
gene. The other pedigree results from deletion of a
paternally imprinted autosomal gene. In both pedigrees,
affected individuals (red symbols) are heterozygous for
the deletion. These individuals are affected because one
copy of the chromosome carries an imprinted, inactive
gene, while the other carries a deletion of the gene. Dotted
yellow symbols indicate individuals that carry the deleted
locus, but do not display the mutant phenotype. Which
pedigree is based on paternal imprinting and which on
maternal imprinting? Explain your answer.
(A)
(B)
7–13 If you insert a β-galactosidase gene lacking its own
transcription control region into a cluster of piRNA genes
in Drosophila, you find that β-galactosidase expression
from a normal copy
Figure
elsewhere
7-35
in the genome is strongly
inhibited in the fly’s germ cells. If the inactive β-galactosidase
gene is inserted Problem outside the 7-83 piRNA gene cluster, the
normal gene is properly expressed. What do you suppose
is the basis for this observation? How would you test your
hypothesis?
A
R
Figure 7-33
Problem 7-79
A
A
activator protein
turns on its own
transcription
R
R
repressor protein
turns off its own
transcription
Figure Q7–3 Pedigrees reflecting maternal and paternal imprinting
(Problem 7–12). In one pedigree, the gene is paternally imprinted; in
the other, it is maternally imprinted. In generations 3 and 4, only one
of the two parents in the indicated matings is shown; the other parent
is a normal individual from outside this pedigree. Affected individuals
are represented by red circles for females and red squares for males.
Dotted yellow symbols indicate individuals that carry the deletion but
do not display the phenotype.