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Genetics Chapter 16 Questions
Terms in this set (23)
C1. What is the difference between a constitutive gene and a regulated
A constitutive gene is unregulated, which means that its expression level
is relatively constant. In contrast, the expression of a regulated gene varies under different
conditions. In bacteria, the regulation of genes often occurs at the level of transcription by
combinations of regulatory proteins and small effector molecules. In addition, gene
expression can be regulated at the level of translation or the function of a protein can be
regulated after translation is completed.
C2. In general, why is it important to regulate genes? Discuss examples
of situations in which it would be advantageous for a bacterial cell
to regulate genes.
In bacteria, gene regulation greatly enhances the efficiency of cell
growth. It takes a lot of energy to transcribe and translate genes. Therefore, a cell is much
more efficient and better at competing in its environment if it expresses genes only when
the gene product is needed. For example, a bacterium will express only the genes that are
necessary for lactose metabolism when a bacterium is exposed to lactose. When the
environment is missing lactose, these genes are turned off. Similarly, when tryptophan
levels are high within the cytoplasm, the genes that are required for tryptophan
biosynthesis are repressed.
C3. If a gene is repressible and under positive control, describe what
kind of effector molecule and regulatory protein are involved.
Explain how the binding of the effector molecule affects the
In this case, an inhibitor molecule and an activator protein are involved.
The binding of the inhibitor molecule to the activator protein would prevent it from
binding to the DNA and thereby inhibit its ability to activate transcription.
C4. Transcriptional regulation often involves a regulatory protein that
binds to a segment of DNA and a small effector molecule that
binds to the regulatory protein. Do the following terms apply to a
regulatory protein, a segment of DNA, or a small effector molecule?
A. Repressor E. Activator
B. Inducer F. Attenuator
C. Operator site G. Inhibitor
A. Regulatory protein
B. Effector molecule
C. DNA segment
D. Effector molecule
E. Regulatory protein
F. DNA segment
G. Effector molecule
C5. An operon is repressible—a small effector molecule turns off
transcription. Which combinations of small effector molecules and
regulatory proteins could be involved?
A. An inducer plus a repressor
B. A corepressor plus a repressor
C. An inhibitor plus an activator
D. An inducer plus an activator
B and C are correct. In both of these cases, the presence of the small
effector molecule will turn off transcription. In contrast, the presence of an inducer turns
C6. Some mutations have a cis-effect on gene expression, whereas
others have a trans-effect. Explain the molecular differences
between cis- and trans-mutations. Which type of mutation (cis or
trans) can be complemented in a merozygote experiment?
A mutation that has a cis-effect is within a genetic regulatory sequence,
such as an operator site, that affects the binding of a genetic regulatory protein. A ciseffect
mutation affects only the adjacent genes that the genetic regulatory sequence
controls. A mutation having a trans-effect is usually in a gene that encodes a genetic
regulatory protein. A trans-effect mutation can be complemented in a merozygote
experiment by the introduction of a normal gene that encodes the regulatory protein.
***C7. What is enzyme adaptation? From a genetic point of view, how
does it occur?
The term enzyme adaptation means that a particular enzyme is made
only when a cell is exposed to the substrate for that enzyme. It occurs because the gene
that encodes the enzyme that is involved in the metabolism of the substrate is expressed
only when the cells have been exposed to the substrate.
C8. In the lac operon, how would gene expression be affected if one of
the following segments was missing?
A. lac operon promoter
B. Operator site
C. lacA gene
A. No transcription would take place. The lac operon could not be expressed.
B. No regulation would take place. The operon would be continuously turned
C. The rest of the operon would function normally but none of the transacetylase
would be made.
C9. If an abnormal repressor protein could still bind allolactose, but
the binding of allolactose did not alter the conformation of the
repressor protein, how would this affect the expression of the lac
It would be impossible to turn the lac operon on even in the presence of
lactose because the repressor protein would remain bound to the operator site.
C10. What is diauxic growth? Explain the roles of cAMP and the
catabolite activator protein (CAP) in this process.
Diauxic growth refers to the phenomenon in which a cell first uses up
one type of sugar (such as glucose) before it begins to metabolize a second sugar (such as
lactose). In this case, it is caused by gene regulation. When a bacterial cell is exposed to
both sugars, the uptake of glucose causes the cAMP levels in the cell to fall. When this
occurs, the catabolite activator protein (CAP) is removed from the lac operon so it is not
able to be activated by CAP.
***C11. Mutations may have an effect on the expression of the lac operon
and the trp operon. Would the following mutations have a cisor
trans-effect on the expression of the structural genes in the
A. A mutation in the operator site that prevents the lac repressor
from binding to it
B. A mutation in the lacI gene that prevents the lac repressor from
binding to DNA
C. A mutation in trpL that prevents attenuation
A. Cis-effect. It would affect only the genes that are in the adjacent operon.
B. Trans-effect. This is a mutation that affects a protein that can move
throughout the cell.
C. Trans-effect. This is a mutation that affects a protein that can move
throughout the cell.
D. Cis-effect. It would affect only the genes that are in the adjacent operon.
C12. Would a mutation that inactivated the lac repressor and prevented
it from binding to the lac operator site result in the constitutive
expression of the lac operon under all conditions? Explain. What
is the disadvantage to the bacterium of having a constitutive lac
A mutation that prevented the lac repressor from binding to the operator
would make the lac operon constitutive only in the absence of glucose. However, this
mutation would not be entirely constitutive because transcription would be inhibited in
the presence of glucose. The disadvantage of constitutive expression of the lac operon is
that the bacterial cell would waste a lot of energy transcribing the genes and translating
the mRNA when lactose was not present.
***C13. What is meant by the term attenuation? Is it an example of gene
regulation at the level of transcription or translation? Explain your
Attenuation means that transcription is ended before it has reached the
end of an operon. Because it causes an end to transcription, it is a form of transcriptional
regulation even though the translation of the trpL region plays a key role in the
***C14. As described in Figure 16.12, four regions within the trpL mRNA
can form stem-loops. Let's suppose that mutations have been
previously identified that prevent the ability of a particular region
to form a stem-loop with a complementary region. For example, a
region 1 mutant cannot form a 1-2 stem-loop, but it can still form
a 2-3 or 3-4 stem-loop. Likewise, a region 4 mutant can form a
1-2 or 2-3 stem-loop but not a 3-4 stem-loop. Under the following
conditions, would attenuation occur?
A. Region 1 is mutant, tryptophan is high, and translation is not
B. Region 2 is mutant, tryptophan is low, and translation is
C. Region 3 is mutant, tryptophan is high, and translation is not
D. Region 4 is mutant, tryptophan is low, and translation is not
A. Attenuation will not occur because loop 2-3 will form.
B. Attenuation will occur because 2-3 cannot form, so 3-4 will form.
C. Attenuation will not occur because 3-4 cannot form.
D. Attenuation will not occur because 3-4 cannot form.
***C15. As described in Chapter 15 , enzymes known as aminoacyl-tRNA
synthetases are responsible for attaching amino acids to tRNAs.
Let's suppose that tryptophanyl-tRNA synthetase was partially
defective at attaching tryptophan to tRNA; its activity was only
10% of that found in a normal bacterium. How would that affect
attenuation of the trp operon? Would it be more or less likely to be
attenuated? Explain your answer.
A defective tryptophanyl-tRNA synthetase would make attenuation less
likely. This is because the bacterial cell would have a lower amount of charged tRNATrp.
Therefore, it would be more likely for the ribosome to stall at the tryptophan codons
found within the trpL gene, even if the concentration of tryptophan amino acids in the
cell was high. When the ribosome stalls at these tryptophan codons, this prevents
***C16. The 3-4 stem-loop and U-rich attenuator found in the trp operon
(see Figure 16.12) is an example of ρ-independent termination. The
mechanism of ρ-independent termination is described in Chapter
14 . Would you expect attenuation to occur if the tryptophan levels
were high and mutations changed the attenuator sequence from
UUUUUUUU to UGGUUGUC? Explain why or why not.
The addition of Gs and Cs into the U-rich sequence would prevent
attenuation. The U-rich sequence promotes the dissociation of the mRNA from the DNA,
when the terminator stem-loop forms. This causes RNA polymerase to dissociate from
the DNA and thereby causes transcriptional termination. The UGGUUGUC sequence
would probably not dissociate because of the Gs and Cs. Remember that GC base pairs
have three hydrogen bonds and are more stable than AU base pairs, which have only two
***C17. Mutations in tRNA genes can create tRNAs that recognize stop
codons. Because stop codons are sometimes called nonsense
codons, these types of mutations that affect tRNAs are called
nonsense suppressors. For example, a normal tRNAGly has an
anticodon sequence CCU that recognizes a glycine codon in
mRNA (GGA) and puts in a glycine during translation. However,
a mutation in the gene that encodes tRNAGly could change the
anticodon to ACU. This mutant tRNAGly would still carry glycine,
but it would recognize the stop codon UGA. Would this mutation
affect attenuation of the trp operon? Explain why or why not.
Note: To answer this question, you need to look carefully at Figure
16.12 and see if you can identify any stop codons that may exist
beyond the UGA stop codon that is found after region 1.
If you look very carefully at the RNA sequence in Figure 16.12, you will
notice that a UAA codon is found just past region 2. Therefore, in this mutant strain, the
UGA stop codon at the end of region 1 could be read by the mutant tRNAGly and then
the ribosome would stop at the UAA codon just past region 2. If the ribosome paused
here, it would probably cover up a portion of region 3, and therefore the terminator 3-4
stem-loop would not form. According to this scenario, attenuation could not occur.
However, we should also keep in mind the issue of timing. The ribosome would have to
be really close to RNA polymerase to prevent attenuation in this nonsense suppressor
strain. It is possible that the 3-4 stem-loop might form before the ribosome reaches the
UAA stop codon just past region 2. Therefore, attenuation might occur anyway because
the 3-4 stem-loop might form before the ribosome reaches the UAA stop codon.
***C18. Translational control is usually aimed at preventing the initiation
of translation. With regard to cellular efficiency, why do you think
this is the case?
It takes a lot of cellular energy to translate mRNA into a protein. A cell
wastes less energy if it prevents the initiation of translation rather than a later stage such
as elongation or termination.
C19. What is antisense RNA? How does it affect the translation of a
Antisense RNA is RNA that is complementary to a functional RNA such
as mRNA. The binding of antisense RNA to mRNA inhibits translation.
***C20. A species of bacteria can synthesize the amino acid histidine so it
does not require histidine in its growth medium. A key enzyme,
which we will call histidine synthetase, is necessary for histidine
biosynthesis. When these bacteria are given histidine in their
growth medium, they stop synthesizing histidine intracellularly.
Based on this observation alone, propose three different regulatory
mechanisms to explain why histidine biosynthesis ceases when
histidine is in the growth medium. To explore this phenomenon
further, you measure the amount of intracellular histidine
synthetase protein when cells are grown in the presence and
absence of histidine. In both conditions, the amount of this protein
is identical. Which mechanism of regulation would be consistent
with this observation?
One mechanism is that histidine could act as corepressor that shuts down
the transcription of the histidine synthetase gene. A second mechanism would be that
histidine could act as an inhibitor via feedback inhibition. A third possibility is that
histidine inhibits the ability of the mRNA encoding histidine synthetase to be translated.
Perhaps it induces a gene that encodes an antisense RNA. If the amount of histidine
synthetase protein was identical in the presence and absence of extracellular histidine, a
feedback inhibition mechanism is favored, because this affects only the activity of the
histidine synthetase enzyme, not the amount of the enzyme. The other two mechanisms
would diminish the amount of this protein.
***C21. Using three examples, describe how allosteric sites are important
in the function of genetic regulatory proteins.
1. lac operon: The binding of allolactose causes a conformational change in the
repressor protein and removes it from the operator site.
2. ara operon: The binding of arabinose to AraC breaks the looping interaction
and leads to the activation of the ara operon.
3. trp operon: The binding of tryptophan to the trp repressor causes it to bind to
the operator site and inhibits transcription.
***C22. In what ways are the actions of the lac repressor and trp repressor
similar and how are they different with regard to their binding to
operator sites, their effects on transcription, and the influences of
small effector molecules?
The two proteins are similar in that both bind to a segment of DNA and
repress transcription. They are different in three ways. (1) They recognize different
effector molecules (i.e., the lac repressor recognizes allolactose, and the trp repressor
recognizes tryptophan. (2) Allolactose causes the lac repressor to release from the
operator, while tryptophan causes the trp repressor to bind to its operator. (3) The
sequences of the operator sites that these two proteins recognize are different from each
other. Otherwise, the lac repressor could bind to the trp operator, and the trp repressor
could bind to the lac operator.
C23. Transcriptional repressor proteins (e.g., lac repressor), antisense
RNA, and feedback inhibition are three different mechanisms that
turn off the expression of genes and gene products. Which of these
three mechanisms would be most effective in each of the following
A. Shutting down the synthesis of a polypeptide
B. Shutting down the synthesis of mRNA
C. Shutting off the function of a protein
For your answers in parts A-C that have more than one
mechanism, which mechanism is the fastest or the most efficient?
A. Antisense RNA or a translational repressor would shut down protein synthesis the
fastest. A transcriptional repressor would also shut down the synthesis of mRNA, so it
would eventually shut down protein synthesis once all of the preexisting mRNA had been
degraded. Feedback inhibition would have no effect on protein synthesis.
B. Only a transcriptional repressor protein would shut down the synthesis of
C. Feedback inhibition is the fastest way to shut down the function of a protein.
Antisense RNA and transcriptional repressors eventually prevent protein function once all
of the preexisting mRNA and protein have been degraded.
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