Unit 6 · 12–16% of the exam Beta

Unit 6 practice test: Gene Expression and Regulation

12 exam-style questions from the unit, free, with an explanation for every option. Sets share one table, graph or experiment, as on the real exam.

Covers: DNA and RNA Structure; Replication; Transcription and RNA Processing; Translation; Regulation of Gene Expression; Gene Expression and Cell Specialization; Mutations; Biotechnology.

Experimental setup

Putting a plasmid into bacteria

A plasmid carries two added genes: one that lets cells survive the drug ampicillin, and one for a protein that glows green. Students mixed 0.10 µg of the plasmid with 1.0 mL of E. coli cells treated to take up DNA (+ plasmid), and set up the same cells without plasmid (− plasmid). After a brief heat shock, 0.10 mL of each mixture was spread on each plate. Colonies were counted after 24 hours.

Growth on each plate
PlateCellsPlate containsResult
1− plasmidNutrients onlyCells cover the plate (a lawn)
2− plasmidNutrients + ampicillinNo colonies
3+ plasmidNutrients onlyA lawn; it does not glow
4+ plasmidNutrients + ampicillin84 colonies, all glowing green

1. Which conclusion is best supported by plates 2 and 4?

  1. Some cells took up the plasmid, whose gene let them survive ampicillin.
  2. Ampicillin causes the cells to take up plasmids that are in the medium around them.
  3. Each cell exposed to the plasmid took it up, and each of them began to glow green.
  4. The glow gene is needed for the cells to survive the ampicillin in the plate.
Show the answer

Cells without plasmid cannot grow on ampicillin (plate 2), but 84 colonies grow from the plasmid mixture (plate 4): those cells were transformed, and the plasmid's gene protects them.

  • Correct: Some cells took up the plasmid, whose gene let them survive ampicillin.: Correct: transformation plus the protective gene.
  • Ampicillin causes the cells to take up plasmids that are in the medium around them.: The plasmid and cells were mixed before plating; ampicillin only kills cells without the plasmid.
  • Each cell exposed to the plasmid took it up, and each of them began to glow green.: Plate 3 shows most cells did not take it up: the lawn there does not glow.
  • The glow gene is needed for the cells to survive the ampicillin in the plate.: The drug-survival gene does that; glowing is a separate trait carried on the same plasmid.

2. Plate 3 has a lawn that does not glow, though those cells were mixed with plasmid. Why?

  1. Few cells took up the plasmid; without ampicillin, untransformed cells grew over them.
  2. Cells do not express the glow gene unless ampicillin is present to switch the gene on.
  3. The plasmid was destroyed by the nutrients on the plates that lacked ampicillin.
  4. The lawn glows, but just after it has been exposed to ampicillin for a whole day.
Show the answer

Transformation is rare. On a plate without ampicillin every cell grows, so the few transformed cells are lost in a lawn of untransformed ones. Ampicillin removes the untransformed cells, which is why the drug-survival gene acts as a selectable marker.

  • Correct: Few cells took up the plasmid; without ampicillin, untransformed cells grew over them.: Correct: without selection, transformants are a tiny minority.
  • Cells do not express the glow gene unless ampicillin is present to switch the gene on.: The glowing colonies on plate 4 show the gene is expressed; nothing suggests ampicillin is needed to switch it on.
  • The plasmid was destroyed by the nutrients on the plates that lacked ampicillin.: Nutrients do not destroy DNA inside cells.
  • The lawn glows, but just after it has been exposed to ampicillin for a whole day.: The lawn does not glow because almost none of its cells have the plasmid.

3. What is the purpose of plate 1?

  1. To show that the cells were alive and able to grow
  2. To show that the plasmid on its own makes cells glow green on plain plates
  3. To count how many cells took up the plasmid in the mixture
  4. To show that ampicillin kills the cells that lack the plasmid
Show the answer

A lawn of untreated cells on plain nutrients confirms the cells survived the treatment and heat shock. Without it, no colonies on plate 2 could mean the cells were dead rather than killed by ampicillin.

  • Correct: To show that the cells were alive and able to grow: Correct: a control for cell survival.
  • To show that the plasmid on its own makes cells glow green on plain plates: Plate 1's cells have no plasmid.
  • To count how many cells took up the plasmid in the mixture: Plate 1 has no plasmid-treated cells; transformants are counted on plate 4.
  • To show that ampicillin kills the cells that lack the plasmid: That is shown by plate 2, compared with plate 1.

Data table

How often mistakes survive DNA copying

The table gives approximate error rates of the kind measured in normal E. coli and in mutants missing one or both correction systems: how often a wrong base remains in the DNA after copying. Proofreading is done by DNA polymerase itself as it adds each nucleotide; mismatch repair is done afterward by other enzymes. The E. coli genome is about 4.6 × 106 base pairs. Values are rounded to the nearest power of ten.

Errors left per base pair copied
StrainProofreadingMismatch repairErrors per base pair copied
NormalWorksWorks1 × 10−10
Mutant PMissingWorks1 × 10−8
Mutant MWorksMissing1 × 10−7
Mutant PMMissingMissing1 × 10−5

4. Which conclusion about the two correction systems is best supported by the table?

  1. Each system removes most errors that reach it, so losing both is far worse than losing one.
  2. Proofreading prevents more errors than mismatch repair, because losing proofreading raises errors the most.
  3. The two systems fix the same errors, so losing both is no worse than losing just one of them.
  4. Mismatch repair does not depend on proofreading happening first, so it fixes nearly any error by itself.
Show the answer

Losing proofreading raises errors 100-fold, losing mismatch repair 1,000-fold, and losing both 100,000-fold (100 × 1,000). Each system catches most of what is left by the step before, so their effects multiply.

  • Correct: Each system removes most errors that reach it, so losing both is far worse than losing one.: Correct: the double mutant is worse than either single mutant by about the other system's factor.
  • Proofreading prevents more errors than mismatch repair, because losing proofreading raises errors the most.: Losing mismatch repair (10−7) raises errors more than losing proofreading (10−8).
  • The two systems fix the same errors, so losing both is no worse than losing just one of them.: Losing both (10−5) is far worse than losing one, so they are not redundant.
  • Mismatch repair does not depend on proofreading happening first, so it fixes nearly any error by itself.: Mutant P, with mismatch repair working, still has 100 times more errors than normal, so mismatch repair does not fix everything.

5. People who inherit a faulty copy of a mismatch repair gene develop colon cancer much more often, and younger, than other people. Which explanation connects this to the table?

  1. Without full mismatch repair, copying errors pile up faster, including in genes that control the cell cycle.
  2. Mismatch repair enzymes directly stop cells from dividing, so without them colon cells divide without control.
  3. Faulty mismatch repair copies DNA faster, so colon cells finish S phase too early and divide too often.
  4. Mismatch repair removes cancer-causing viruses from the DNA, so without it the viruses stay in colon cells.
Show the answer

Mutant M shows that losing mismatch repair raises the error rate about 1,000-fold. In a tissue whose cells divide often, like the colon lining, more errors reach genes such as tumor suppressors and the genes that drive the cell cycle (topic 4.6).

  • Correct: Without full mismatch repair, copying errors pile up faster, including in genes that control the cell cycle.: Correct: a higher mutation rate makes the changes that cause cancer more likely.
  • Mismatch repair enzymes directly stop cells from dividing, so without them colon cells divide without control.: Mismatch repair fixes base errors; it is not a checkpoint protein that holds the cycle.
  • Faulty mismatch repair copies DNA faster, so colon cells finish S phase too early and divide too often.: The table shows accuracy, not speed; nothing suggests copying gets faster.
  • Mismatch repair removes cancer-causing viruses from the DNA, so without it the viruses stay in colon cells.: Mismatch repair corrects mispaired bases in new DNA; it has nothing to do with removing viruses.

6. How does proofreading differ from mismatch repair?

  1. Proofreading is done by DNA polymerase as it builds; mismatch repair fixes errors left after copying.
  2. Proofreading fixes damage from chemicals and radiation; mismatch repair fixes errors made by DNA ligase.
  3. Proofreading checks the old template; mismatch repair checks the RNA primers before they are removed.
  4. Proofreading happens after the whole chromosome is copied; mismatch repair happens at the replication fork.
Show the answer

DNA polymerase checks each base it adds and removes a wrong one before moving on. Mismatch repair enzymes later find mispaired bases, cut out a stretch of the new strand and fill it in again.

  • Correct: Proofreading is done by DNA polymerase as it builds; mismatch repair fixes errors left after copying.: Correct: same goal, different time and different enzymes.
  • Proofreading fixes damage from chemicals and radiation; mismatch repair fixes errors made by DNA ligase.: Both systems fix copying mistakes (mispaired bases), and ligase does not add bases.
  • Proofreading checks the old template; mismatch repair checks the RNA primers before they are removed.: Both systems act on the new strand, which is the one with the copying mistake.
  • Proofreading happens after the whole chromosome is copied; mismatch repair happens at the replication fork.: This reverses the timing: proofreading happens as each base is added, at the fork.

7. Histone proteins carry many amino acids with positively charged side chains, such as lysine and arginine. How does this help histones package DNA?

  1. The positive charges attract DNA's negatively charged phosphate groups along the backbone.
  2. The positive charges pair with the bases in the middle of the helix, holding the strands together.
  3. The positive charges repel the DNA, pushing it into a tightly folded shape.
  4. The positive charges form covalent bonds with the sugars in DNA's backbone.
Show the answer

Each nucleotide's phosphate carries a negative charge, so DNA's outside is strongly negative. Positively charged side chains attract it, letting the DNA wrap tightly around the histone core.

  • Correct: The positive charges attract DNA's negatively charged phosphate groups along the backbone.: Correct: opposite charges attract (ionic interactions).
  • The positive charges pair with the bases in the middle of the helix, holding the strands together.: The bases pair with each other inside the helix; histones contact the backbone on the outside.
  • The positive charges repel the DNA, pushing it into a tightly folded shape.: Repulsion would push DNA away from histones, not wrap it around them.
  • The positive charges form covalent bonds with the sugars in DNA's backbone.: The attraction is ionic and can loosen when charges change; histones do not bond covalently to the sugars.

8. A gene is transcribed in a human cell, but its RNA product is never used as instructions for building a protein. Which kind of RNA could the product be?

  1. tRNA, which folds up and carries amino acids to ribosomes
  2. mRNA, which leaves the nucleus after its introns are removed
  3. pre-mRNA from a gene such as the one for insulin
  4. The exons joined together after splicing of a pre-mRNA
Show the answer

Some genes make RNAs that work as RNA. tRNA folds into a compact shape and brings amino acids to the ribosome; ribosomal RNA forms much of the ribosome itself.

  • Correct: tRNA, which folds up and carries amino acids to ribosomes: Correct: tRNA is a working RNA, not a set of instructions.
  • mRNA, which leaves the nucleus after its introns are removed: mRNA is by definition the RNA that carries a protein's instructions.
  • pre-mRNA from a gene such as the one for insulin: Pre-mRNA is processed into mRNA, which is then used to build a protein.
  • The exons joined together after splicing of a pre-mRNA: Joined exons are mature mRNA, used to build a protein.

9. Bacteria given the human gene for insulin (without introns) make a protein with the same amino acid sequence as human insulin. Which broader conclusion does this support?

  1. Bacteria and humans read codons with nearly the same genetic code, evidence of common ancestry.
  2. Bacteria and humans make the same proteins, because they share the same genes.
  3. Bacteria can splice human genes, because their spliceosomes resemble human ones.
  4. Insulin is a bacterial protein that humans gained from bacteria living in the gut.
Show the answer

The bacterial ribosomes, tRNAs and synthetases turned the human codons into the human amino acid sequence, so the two read the code the same way. A shared, nearly universal code is best explained by descent from a common ancestor.

  • Correct: Bacteria and humans read codons with nearly the same genetic code, evidence of common ancestry.: Correct: same code, shared ancestry.
  • Bacteria and humans make the same proteins, because they share the same genes.: Bacteria do not normally make insulin; the point is that they read the human gene correctly.
  • Bacteria can splice human genes, because their spliceosomes resemble human ones.: The stem says the gene was given without introns; bacteria lack spliceosomes.
  • Insulin is a bacterial protein that humans gained from bacteria living in the gut.: Insulin is an animal hormone; the bacteria made it only because they were given the gene.

10. A mutation changes the lac repressor so that it can no longer bind the operator. Predict β-galactosidase levels in this strain grown on glycerol with no lactose.

  1. High, because nothing blocks RNA polymerase, so the operon is copied without lactose
  2. Near zero, because the repressor is needed to help RNA polymerase bind the promoter
  3. Near zero, because allolactose is still needed to start the operon
  4. Normal for glycerol medium, because the repressor gene is not part of the operon
Show the answer

Lactose normally works only by pulling the repressor off the operator. If the repressor cannot bind, the operon is on whether or not lactose is present (and cAMP is high on glycerol).

  • Correct: High, because nothing blocks RNA polymerase, so the operon is copied without lactose: Correct: a repressor that cannot bind leaves the operon always on.
  • Near zero, because the repressor is needed to help RNA polymerase bind the promoter: The repressor blocks RNA polymerase; it does not help it bind.
  • Near zero, because allolactose is still needed to start the operon: The inducer's only job is to remove the repressor, which is already off the DNA.
  • Normal for glycerol medium, because the repressor gene is not part of the operon: The repressor gene is outside the operon, but its protein controls the operon, so a broken repressor matters.

11. Pancreatic cells translate insulin as a single longer chain, proinsulin. Enzymes in the Golgi and secretory vesicles cut out a middle piece, leaving two chains joined by disulfide bonds; only this form is active. What kind of regulation is this?

  1. Post-translational modification: the protein is changed after it is made
  2. Post-transcriptional regulation, because the mRNA for insulin is spliced in the Golgi
  3. Epigenetic regulation, because the insulin gene's histones are acetylated
  4. Transcriptional regulation, because the insulin gene's enhancer is activated
Show the answer

Cutting a finished polypeptide to activate it is a post-translational modification, like adding phosphate groups or sugars; it controls when and where the active protein appears.

  • Correct: Post-translational modification: the protein is changed after it is made: Correct: the change happens to the protein, after translation.
  • Post-transcriptional regulation, because the mRNA for insulin is spliced in the Golgi: Splicing happens to pre-mRNA in the nucleus, not to proteins in the Golgi.
  • Epigenetic regulation, because the insulin gene's histones are acetylated: Histone marks affect transcription, not the processing of a protein.
  • Transcriptional regulation, because the insulin gene's enhancer is activated: Enhancers act on transcription; this cut happens to the finished chain.

12. A chromosome's genes are normally in the order A-B-C-D-E-F-G. In a mutant chromosome the order is A-B-E-D-C-F-G. What kind of change is this?

  1. Inversion
  2. Duplication
  3. Deletion
  4. Translocation
Show the answer

The segment C-D-E has been flipped end to end into E-D-C, with no genes gained or lost: an inversion.

  • Correct: Inversion: Correct: a reversed segment.
  • Duplication: A duplication would repeat a segment, such as A-B-C-D-C-D-E-F-G.
  • Deletion: A deletion would lose genes, such as A-B-E-F-G.
  • Translocation: A translocation moves a segment to a different, nonhomologous chromosome.

Keep going

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Practice has every question in the unit, with feedback after each one; the notes for every topic are free. Write a full answer with the justification trainer. Other units: Unit 1 · Unit 2 · Unit 3 · Unit 4 · Unit 5 · Unit 6 · Unit 7 · Unit 8.