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Table of contents

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1. Introduction to Genetics51m
2. Mendel's Laws of Inheritance3h 37m
3. Extensions to Mendelian Inheritance2h 41m
4. Genetic Mapping and Linkage2h 28m
5. Genetics of Bacteria and Viruses1h 21m
6. Chromosomal Variation1h 48m
7. DNA and Chromosome Structure56m
8. DNA Replication1h 10m
9. Mitosis and Meiosis1h 34m
10. Transcription1h 0m
11. Translation58m
12. Gene Regulation in Prokaryotes1h 19m
13. Gene Regulation in Eukaryotes44m
14. Genetic Control of Development44m
15. Genomes and Genomics1h 50m
16. Transposable Elements47m
17. Mutation, Repair, and Recombination1h 6m
18. Molecular Genetic Tools19m
- Genetic Cloning
  9m
- Methods for Analyzing DNA
  9m
19. Cancer Genetics29m
- Overview of Cancer
  21m
- Cancer Mutations
  7m
20. Quantitative Genetics1h 26m
21. Population Genetics50m
- Hardy Weinberg
  19m
- Allelic Frequency Changes
  31m
22. Evolutionary Genetics29m

17. Mutation, Repair, and Recombination

DNA Repair

17. Mutation, Repair, and Recombination

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DNA Proofreading

Kylia Goodner

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Hi. In this video, we're going to be talking about DNA repair. So, DNA damage occurs often, and it's repaired in a lot of different ways. So, one of the or a couple of the ones that we've talked about previously, the first is DNA proofreading, and DNA proofreading is just the process of repairing a nucleotide that's been added in error, and so it repairs a mispaired base. And so this is one that we've already talked about and is a major part in repairing that damaged DNA. There are other ways that are maybe less specific. We're going to talk about individual pathways, but I did want to throw this other pathway in, and this is just that there are a lot of different enzymes that can reverse the damage of DNA. So, for instance, there's an enzyme, CPD photolyase, and this is an enzyme that repairs dimers caused from UV light. So, UV light, it hits our skin anytime we go outside. It's going to cause dimers, and there are these enzymes in there that go and repair this. Then there's enzymes forced to every type of specific DNA. And these kind of exist, I mean, of course, they're pathways, but they exist outside of the major pathways that we're going to talk about later. So, these are kind of the first two, just like summarizing different ways that DNA damage can be repaired. So here's an example of proofreading. We have DNA polymerase. This is being copied. There's some type of error that happens here, where C is paired with T, not supposed to be proofreading, goes back, excises that C, and makes the correct TA pairing as it extends forward. So that is one major way that DNA damage is repaired. Let's turn the page and talk about more specific pathways.

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Related Videos

Related Practice

Textbook Question

Write a short essay contrasting how these concepts may differ between bacteria and eukaryotes.

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

Identify two mechanisms that can correct the kind of abnormality resulting from the circumstances identified in part (c).

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

If a DNA replication error is detected by DNA polymerase, how is it corrected?

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

DNA mismatch repair can accurately distinguish between the template strand and the newly replicated strand of a DNA duplex. What characteristic of DNA strands is used to make this distinction?

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

If the kind of abnormality identified in part (c) is not corrected before the next DNA replication cycle, what kind of mutation occurs?

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

If a replication error escapes detection and correction, what kind of abnormality is most likely to exist at the site of replication error?

Textbook Question

Answer the following questions concerning the accuracy of DNA polymerase during replication.

What general mechanism do DNA polymerases use to check the accuracy of DNA replication and identify errors during replication?

Textbook Question

DNA damage brought on by a variety of natural and artificial agents elicits a wide variety of cellular responses involving numerous signaling pathways. In addition to the activation of DNA repair mechanisms, there can be activation of pathways leading to apoptosis (programmed cell death) and cell-cycle arrest. Why would apoptosis and cell-cycle arrest often be part of a cellular response to DNA damage?

Textbook Question

Contrast the various types of DNA repair mechanisms known to counteract the effects of UV radiation. What is the role of visible light in repairing UV-induced mutations?

Textbook Question

A 1-mL sample of the bacterium E. coli is exposed to ultraviolet light. The sample is used to inoculate a 500-mL flask of complete medium that allows growth of all bacterial cells. The 500-mL culture is grown on the benchtop, and two equal-size samples are removed and plated on identical complete-medium growth plates. Plate 1 is immediately wrapped in a dark cloth, but plate 2 is not covered. Both plates are left at room temperature for 36 hours and then examined. Plate 2 is seen to contain many more growing colonies than plate 1. Thinking about DNA repair processes, how do you explain this observation?

Textbook Question

A strain of E. coli is identified as having a null mutation of the RecA gene. What biological property do you expect to be absent in the mutant strain? What is the molecular basis for the missing property?

Textbook Question

It has been shown that infectious agents such as viruses often exert a dramatic effect on their host cell's genome architecture. In many cases, viruses induce methylation of host DNA sequences in order to enhance their infectivity. What specific host gene functions would you consider as strong candidates for such methylation by infecting viruses?

Textbook Question

Xeroderma pigmentosum (XP) is an autosomal recessive condition characterized by moderate to severe sensitivity to ultraviolet (UV) light. Patients develop multiple skin lesions on UV-exposed skin, and skin cancers often develop as a result. XP is caused by deficient repair of DNA damage from UV exposure. Many genes are known to be involved in repair of UV-induced DNA damage, and several of these genes are implicated in XP. What genetic phenomenon is illustrated by XP?

Textbook Question

You have identified five genes in S. cerevisiae that are induced when the yeast are grown in a high-salt (NaCl) medium. To study the potential roles of these genes in acclimation to growth in high-salt conditions, you wish to examine the phenotypes of loss- and gain-of-function alleles of each. How would your answer differ if you were working with tomato plants instead of yeast?

Textbook Question

You have identified five genes in S. cerevisiae that are induced when the yeast are grown in a high-salt (NaCl) medium. To study the potential roles of these genes in acclimation to growth in high-salt conditions, you wish to examine the phenotypes of loss- and gain-of-function alleles of each. How will you do this?

Textbook Question

The SOS repair genes in E. coli (discussed in Chapter 15) are negatively regulated by the lexA gene product, called the LexA repressor. When a cell's DNA sustains extensive damage, the LexA repressor is inactivated by the recA gene product (RecA), and transcription of the SOS genes is increased dramatically. One of the SOS genes is the uvrA gene. You are a student studying the function of the uvrA gene product in DNA repair. You isolate a mutant strain that shows constitutive expression of the UvrA protein. Naming this mutant strain uvrAᶜ, you construct the diagram shown above in the right-hand column showing the lexA and uvrA operons: Outline a series of genetic experiments that would use partial diploid strains to determine which of the two possible mutations you have isolated.

Textbook Question

Describe the 'end-replication problem' in eukaryotes. How is it resolved?

Textbook Question

A fellow student considers the issues in Problem 22 and argues that there is a more straightforward, nongenetic experiment that could differentiate between the two types of mutations. The experiment requires no fancy genetics and would allow you to easily assay the products of the other SOS genes. Propose such an experiment.

Textbook Question

Many of the gene products involved in DNA synthesis were initially defined by studying mutant E. coli strains that could not synthesize DNA. The dnaQ gene encodes the ε subunit of DNA polymerase. What effect is expected from a mutation in this gene?

Textbook Question

Many of the gene products involved in DNA synthesis were initially defined by studying mutant E. coli strains that could not synthesize DNA. The dnaE gene encodes the α subunit of DNA polymerase III. What effect is expected from a mutation in this gene? How could the mutant strain be maintained?

Textbook Question

When a double-strand DNA break occurs in a eukaryotic cell, it may be repaired by either nonhomologous end joining or homologous recombination. How do these different repair mechanisms lead to potentially different outcomes?

Textbook Question

Using your knowledge of DNA repair pathways, choose the pathway that would be used to repair the following types of DNA damage. Explain your reasoning.

a change in DNA sequence caused by a mistake made by DNA polymerase during replication

Textbook Question

Using your knowledge of DNA repair pathways, choose the pathway that would be used to repair the following types of DNA damage. Explain your reasoning.

heavily damaged bacterial DNA

Textbook Question

Ataxia telangiectasia (OMIM 208900) is a human inherited disorder characterized by poor coordination (ataxia), red marks on the face (telangiectasia), increased sensitivity to X-rays and other radiation, and an increased susceptibility to cancer. Recent studies have shown that this disorder occurs as a result of mutation of the ATM gene. Propose a mechanism for how a mutation in the ATM gene leads to the characteristics associated with the disorder. Be sure to relate the symptoms of this disorder to functions of the ATM protein. Further, explain why DNA repair mechanisms cannot correct this problem.

Textbook Question

A geneticist searching for mutations uses the restriction endonucleases SmaI and PvuII to search for mutations that eliminate restriction sites. SmaI will not cleave DNA with CpG methylation. It cleaves DNA at the restriction digestion sequence ↓ 5′−CCC GGG−3′ 3′−GGG CCC−3′ ↑ PvuII is not sensitive to CpG methylation. It cleaves DNA at the restriction sequence ↓ 5′−CAG CTG−3′ 3′−GTC GAC−5′ ↑ Explain why CpG dinucleotides are hotspots of mutation.

Textbook Question

A geneticist searching for mutations uses the restriction endonucleases SmaI and PvuII to search for mutations that eliminate restriction sites. SmaI will not cleave DNA with CpG methylation. It cleaves DNA at the restriction digestion sequence ↓ 5′−CCC GGG−3′ 3′−GGG CCC−3′ ↑ PvuII is not sensitive to CpG methylation. It cleaves DNA at the restriction sequence ↓ 5′−CAG CTG−3′ 3′−GTC GAC−5′ ↑ What process is the researcher intending to detect with the use of these restriction enzymes?

Textbook Question

A geneticist searching for mutations uses the restriction endonucleases SmaI and PvuII to search for mutations that eliminate restriction sites. SmaI will not cleave DNA with CpG methylation. It cleaves DNA at the restriction digestion sequence ↓ 5′−CCC GGG−3′ 3′−GGG CCC−3′ ↑ PvuII is not sensitive to CpG methylation. It cleaves DNA at the restriction sequence ↓ 5′−CAG CTG−3′ 3′−GTC GAC−5′ ↑ What common feature do SmaI and PvuII share that would be useful to a researcher searching for mutations that disrupt restriction digestion?

Textbook Question

In a mouse-breeding experiment a new mutation called Dumbo is identified. A mouse with the Dumbo mutation has very large ears. It is produced by two parental mice with normal ear size. Based on this information, can you tell whether the Dumbo mutation is a regulatory mutation or a mutation of a protein-coding gene? Why or why not?

Textbook Question

Considering the Dumbo mutation in Problem 37, what kinds of additional evidence would help you determine whether Dumbo is a mutation of a regulatory sequence or of a protein-coding gene?

Textbook Question

Thinking back to the discussion of gain-of-function and loss-of-function mutations in Section 4.1, and putting those concepts together with the discussion of base substitution mutations in this chapter, explain why gain-of-function mutations are often dominant and why loss-of-function mutations are often recessive. Give an example of a type of gain-of-function mutation that is dominant and of a loss-of-function mutation that is recessive.

Multiple Choice

Which of the following repair pathways repairs damage that causes distortions in the double helix?

Multiple Choice

Which of the following repair pathways uses a methylated strand of DNA to correct DNA damage?

Multiple Choice

True or False:Translesion DNA synthesis is the first mechanism the cell uses to repair DNA damage?

Multiple Choice

Which of the following pathways is an error-free way to repair double-stranded breaks?

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