Unit 7: DNA Structure, Replication, Mutation, and Repair
The molecule's own architecture, how it copies itself with almost no errors, and what happens on the rare occasions it doesn't.
9 topics · 33 questions
Each topic is a path, not a menu: work down it in order and every question builds on the one above. Click any of them to watch the answer draw itself.
The DNA Double Helix
- How it worksHow do complementary base pairing and the antiparallel backbone hold the double helix together?
- Common mistakeWhy doesn't the ratio of A to T or G to C in DNA ever depend on the species?
- Going furtherWhat happens to the double helix's stability when its GC content is higher than its AT content?
Your turn1 of 2
Across every species examined, from bacteria to humans, the amount of adenine always equals the amount of thymine, and the amount of guanine always equals the amount of cytosine (Chargaff's rules), even though the OVERALL GC content varies widely between species. Why does this A-to-T and G-to-C equality never depend on the species?Semiconservative Replication and the Meselson-Stahl Experiment
- How it worksHow does each parental strand serve as a template for building one new complementary strand?
- Worked exampleTrace the density bands Meselson and Stahl expected after one and two rounds of replication under semiconservative, conservative, and dispersive models.
- Common mistakeWhy doesn't conservative replication match the actual density-gradient results from bacterial DNA?
- Going furtherWhat happens to the density-gradient bands after a third round of replication under the semiconservative model?
Your turn1 of 2
Starting from DNA made entirely of heavy nitrogen, bacteria are allowed to replicate semiconservatively for 5 generations in a light-nitrogen medium. Each original heavy strand is conserved forever, pairing with one new light strand each round, while newly made duplexes from light-light strands keep doubling. What fraction of all DNA duplexes after 5 generations are fully light (light-light)?The Replication Fork: Leading and Lagging Strands
- How it worksHow does DNA polymerase's requirement to add bases only in one direction force the lagging strand into Okazaki fragments?
- Worked exampleTrace the direction of synthesis on both template strands as a replication fork opens up.
- Common mistakeWhy doesn't the lagging strand mean that half of a cell's DNA replicates slower than the other half?
Your turn1 of 2
At a replication fork, DNA polymerase can only add new bases in the 5' to 3' direction. One template strand allows continuous synthesis, but the other must be copied in short, disconnected pieces (Okazaki fragments) that are stitched together afterward. How does this one directional rule force that difference?Enzymes of DNA Replication
- How it worksHow do helicase, primase, DNA polymerase, and ligase each perform one specific step of replication?
- Worked exampleTrace the role of DNA polymerase's proofreading function in removing a mismatched base right after it is added.
- Going furtherWhat happens to a growing DNA strand at a replication fork if DNA ligase is missing?
- Worked exampleFind how many Okazaki fragments must be joined given a lagging strand template of 3000 bases synthesized in 150-base fragments.
- Common mistakeWhy doesn't DNA polymerase start building a new strand from scratch without help from primase?
Your turn1 of 2
A lagging strand template of 4634 bases is synthesized as a series of Okazaki fragments, each about 230 bases long. Approximately how many Okazaki fragments must be joined together by DNA ligase to complete this strand?Types of Point Mutation
- How it worksHow does a single base substitution turn into a silent, missense, or nonsense mutation depending on where it falls in the codon?
- Worked exampleFind the effect of changing the DNA triplet GGA to GGG given both code for glycine.
- Worked exampleFind the effect of changing the DNA triplet TAC to TAA on the protein product.
- Common mistakeWhy doesn't every base change in a gene automatically change the amino acid it codes for?
Your turn1 of 2
A point mutation changes a codon from GGA to GGG. Both GGA and GGG code for the amino acid glycine. What type of mutation is this, and what does it do to the protein?Frameshift Mutations
- How it worksHow does inserting or deleting a number of bases not divisible by three shift every codon that follows it?
- Worked exampleFind how a single base insertion shifts the reading frame of the sequence ATG CAT CAT CAT into a new set of codons.
- Common mistakeWhy doesn't deleting exactly three bases in a row cause a frameshift?
Your turn1 of 2
The coding sequence ATG CAT CAT CAT (coding for Met-His-His-His) has a single extra base inserted right after the initial ATG, giving ATG XCA TCA TCA T (where X is the inserted base). What happens to every codon downstream of the insertion point?Mutagens and How They Cause Mutation
- How it worksHow does ultraviolet light fuse two adjacent thymine bases into a pyrimidine dimer?
- How it worksHow does a base analog like 5-bromouracil get mistakenly incorporated into DNA and cause a mutation on the next replication?
- Going furtherWhat happens to a cell's mutation rate when it is exposed to both UV light and a chemical mutagen at the same time?
Your turn1 of 2
Ultraviolet light causes a very specific, predictable type of DNA damage rather than random breaks scattered throughout the genome. What exactly does UV light do to cause this damage?DNA Repair Mechanisms
- How it worksHow does mismatch repair distinguish the newly synthesized strand from the template strand to fix a replication error?
- How it worksHow does nucleotide excision repair cut out and replace a UV-induced thymine dimer?
- Worked exampleTrace how homologous recombination repairs a double-strand break using the sister chromatid as a template.
- Common mistakeWhy doesn't a cell with a broken DNA repair gene die immediately instead of accumulating mutations over time?
- Going furtherWhat happens to a cell's mutation rate over many generations when its own mismatch repair gene is mutated?
Your turn1 of 2
After DNA replication, mismatch repair enzymes scan the new DNA for base-pairing errors DNA polymerase's proofreading missed. To fix a mismatch correctly, the repair system must cut out the WRONG base — but both strands have the correct sequence everywhere else, so how does it know which of the two mismatched bases is the new (likely wrong) one rather than the original template?Repair-Deficiency Disorders: Xeroderma Pigmentosum
- How it worksHow does a defective nucleotide excision repair gene leave unrepaired thymine dimers to accumulate in skin cells?
- Ties togetherHow does xeroderma pigmentosum connect a single faulty repair gene to a dramatically higher skin cancer rate?
- Going furtherWhat happens to a xeroderma pigmentosum patient's mutation rate in cells that are never exposed to UV light at all?
Your turn1 of 2
People with xeroderma pigmentosum carry a mutation in a nucleotide excision repair gene and develop skin cancer at dramatically higher rates than the general population. How does one faulty repair gene connect to such a large increase in cancer risk?