Section 12.2
17.For each of the following types of transcriptional control, indicate whether the protein produced by the regulator gene will be synthesized initially as an active repressor, inactive repressor, active activator, or inactive activator.
Negative control in a repressible operon
Positive control in a repressible operon
Negative control in an inducible operon
Positive control in an inducible operon
*18.A mutation at the operator prevents the regulator protein from binding. What effect will this mutation have in the following types of operons?
Regulator protein is a repressor in a repressible operon.
Regulator protein is a repressor in an inducible operon.
19.The blob operon produces enzymes that convert compound A into compound B. The operon is controlled by a regulatory gene S. Normally, the enzymes are synthesized only in the absence of compound B. If gene S is mutated, the enzymes are synthesized in the presence and in the absence of compound B. Does gene S produce a repressor or an activator? Is this operon inducible or repressible?
*20.A mutation prevents the catabolite activator protein (CAP) from binding to the promoter in the lac operon. What will the effect of this mutation be on the transcription of the operon?
21.Under which of the following conditions would a lac operon produce the greatest amount of β-galactosidase? The least? Explain your reasoning.
Lactose present | Glucose present | |
---|---|---|
Condition 1 | Yes | No |
Condition 2 | No | Yes |
Condition 3 | Yes | Yes |
Condition 4 | No | No |
22.A mutant strain of E. coli produces β-galactosidase in the presence and in the absence of lactose. Where in the operon might the mutation in this strain be located?
23.Examine Figure 12.7. What would be the effect of a drug that altered the structure of allolactose so that it was unable to bind to the regulator protein?
24.For E. coli strains with the lac genotypes given below, use a plus sign (+) to indicate the synthesis of β-galactosidase and permease and a minus sign (−) to indicate no synthesis of the proteins.
Lactose absent | Lactose present | |||
---|---|---|---|---|
Genotype of strain | β-Galactosidase | Permease | β-Galactosidase | Permease |
lacI+ lacP+ lacO+ lacZ+ lacY+ | ||||
lacI− lacP+ lacO+ lacZ+ lacY+ | ||||
lacI+ lacP+ lacOc lacZ+ lacY+ | ||||
lacI− lacP+ lacO+ lacZ+ lacY− | ||||
lacI− lacP− lacO+ lacZ+ lacY+ | ||||
lacI+ lacP+ lacO+ lacZ− lacY+/lacI− lacP+ lacO+ lacZ+ lacY− | ||||
lacI− lacP+ lacOc lacZ+ lacY+/lacI+ lacP+ lacO+ lacZ− lacY− | ||||
lacI− lacP+ lacO+ lacZ+ lacY−/lacI+ lacP− lacO+ lacZ− lacY+ | ||||
lacI+ lacP− lacOc lacZ− lacY+/lacI− lacP+ lacO+ lacZ+ lacY− | ||||
lacI+ lacP+ lacO+ lacZ+ lacY+/lacI+ lacP+ lacO+ lacZ+ lacY+ | ||||
lacIs lacP+ lacO+ lacZ+ lacY−/lacI+ lacP+ lacO+ lacZ− lacY+ | ||||
lacIs lacP− lacO+ lacZ− lacY+/lacI+ lacP+ lacO+ lacZ+ lacY+ |
25.Give all possible genotypes of a lac operon that produces β-galactosidase and permease under the following conditions. Do not give partial-
Lactose absent | Lactose present | |||
---|---|---|---|---|
β-Galactosidase | Permease | β-Galactosidase | Permease | |
a. | − | − | + | + |
b. | − | − | − | + |
c. | − | − | + | − |
d. | + | + | + | + |
e. | − | − | − | − |
f. | + | − | + | − |
g. | − | + | − | + |
*26.Explain why mutations in the lacI gene are trans in their effects, but mutations in the lacO gene are cis in their effects.
27.The mmm operon, which has sequences A, B, C, and D (which may be structural genes or regulatory sequences), encodes enzymes 1 and 2. Mutations in sequences A, B, C, and D have the following effects, where a plus sign (+) indicates that the enzyme is synthesized and a minus sign (−) indicates that the enzyme is not synthesized.
Mmm absent | Mmm present | |||
---|---|---|---|---|
Mutation in sequence | Enzyme 1 | Enzyme 2 | Enzyme 1 | Enzyme 2 |
No mutation | + | + | − | − |
A | − | + | − | − |
B | + | + | + | + |
C | + | − | − | − |
D | − | − | − | − |
Is the mmm operon inducible or repressible?
Indicate which sequence (A, B, C, or D) is part of the following components of the operon:
Regulator gene | _____________ |
Promoter | _____________ |
Structural gene for enzyme 1 | _____________ |
Structural gene for enzyme 2 | _____________ |
28. Ellis Engelsberg and his coworkers examined the regulation of genes taking part in the metabolism of arabinose, a sugar (E. Engelsberg et al. 1965. Journal of Bacteriology 90:946–957). Four structural genes encode enzymes that help metabolize arabinose (genes A, B, D, and E). An additional gene C is linked to genes A, B, and D. These genes are in the order D-
Genotype | Arabinose absent | Arabinose present | |
---|---|---|---|
1. | C+ A+ | − | + |
2. | C− A+ | − | − |
3. | C− A+/C+ A− | − | + |
4. | Cc A−/C− A+ | + | + |
On the basis of the results of these experiments, is the C gene an operator or a regulator gene? Explain your reasoning.
Do these experiments suggest that the arabinose operon is negatively or positively controlled? Explain your reasoning.
What type of mutation is Cc?
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29. In E. coli, three structural genes (A, D, and E) encode enzymes A, D, and E, respectively. Gene O is an operator. The genes are in the order O-
Amount of enzyme produced | ||||
---|---|---|---|---|
Genotype | E | D | A | |
1. | E+ D+ A+ O+/ | 2.40 | 2.00 | 3.50 |
E+ D+ A+ O+ | ||||
2. | E+ D+ A+ O−/ | 35.80 | 38.60 | 46.80 |
E+ D+ A+ O+ | ||||
3. | E+ D− A+ O−/ | 1.80 | 1.00 | 47.00 |
E+ D+ A− O+ | ||||
4. | E+ D+ A− O−/ | 35.30 | 38.00 | 1.70 |
E+ D− A+ O+ | ||||
5. | E− D+ A+ O−/ | 2.38 | 38.00 | 46.70 |
E+ D− A+ O+ |
Is the regulator protein that binds to the operator of this operon a repressor (negative control) or an activator (positive control)? Explain your reasoning.
Are genes A, D, and E all under the control of operator O? Explain your reasoning.
Propose an explanation for the low level of enzyme E produced in genotype 3.
Section 12.3
30.A geneticist is trying to determine how many genes are found in a 300,000-
31.In a line of human cells grown in culture, a geneticist isolates a temperature-
32.X31b is an experimental compound that is taken up by rapidly dividing cells. Research has shown that X31b stimulates the methylation of DNA. Some cancer researchers are interested in testing X31b as a possible drug for treating prostate cancer. Offer a possible explanation for why X31b might be an effective anticancer drug.
33.What would be the effect of moving the insulator shown in Figure 12.18 to a position between enhancer II and the promoter for gene B?
*34.An enhancer is surrounded by four genes (A, B, C, and D), as shown in the diagram below. An insulator lies between gene C and gene D. On the basis of the positions of the genes, the enhancer, and the insulator, the transcription of which genes is most likely to be stimulated by the enhancer? Explain your reasoning.
35.Some eukaryotic mRNAs have an AU-
36.A strain of Arabidopsis thaliana possesses a mutation in the APETALA2 gene, in which much of the 3′ untranslated region of mRNA transcribed from the gene is deleted. What is the most likely effect of this mutation on the expression of the APETALA2 gene?
Section 12.4
*37.How do epigenetic traits differ from traditional genetic traits, such as the differences in color and shape of peas that Mendel studied?
*38.A scientist does an experiment in which she removes the offspring of rats from their mother at birth and has her genetics students feed and rear the offspring. Assuming that the students do not lick and groom the baby rats like their mothers normally do, what long-
39. Pregnant female rats were exposed to a daily dose of 100 or 200 mg/kg of vinclozolin, a fungicide commonly used in the wine industry (M. D. Anway et al. 2005, Science 308:1466–1469). The F1 offspring of the exposed females were interbred, producing F2, F3, and F4 rats. None of the F2, F3, or F4 rats were exposed to vinclozolin. Testes from the F1–F4 male rats were examined and compared with those of control rats descended from females that had not been exposed to vinclozolin. There were higher percentages of apoptotic cells (cells that underwent controlled cell death) in the testes of F1–F4 male descendants of females who were exposed to vinclozolin than in descendants of control females (graph a). Furthermore, sperm numbers (graph b) and motilities (graph c) were lower in the F1–F4 descendants of vinclozolin-