Table of contents

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

Genetics

17. Mutation, Repair, and Recombination

DNA Repair

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2:20 minutes

Problem 37

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?

Verified step by step guidance

Step 1: Begin by understanding the nature of the Dumbo mutation. The mutation results in a phenotype (large ears) that is different from the parental phenotype (normal ears). This indicates that the mutation affects gene expression or protein function.

Step 2: Consider the possibility of a regulatory mutation. Regulatory mutations typically affect the expression levels, timing, or location of a gene's activity. If the Dumbo mutation alters the expression of a gene involved in ear development, it could be a regulatory mutation.

Step 3: Consider the possibility of a mutation in a protein-coding gene. Mutations in protein-coding genes can change the structure or function of the protein itself, potentially leading to altered development or morphology, such as large ears.

Step 4: Evaluate the inheritance pattern. Since the Dumbo phenotype arises from two normal-eared parents, this suggests the mutation may be recessive. Both regulatory mutations and protein-coding mutations can exhibit recessive inheritance, so this does not conclusively distinguish between the two types.

Step 5: Conclude that based on the given information, it is not possible to definitively determine whether the Dumbo mutation is regulatory or protein-coding. Additional experiments, such as gene expression analysis or sequencing, would be required to identify the exact nature of the mutation.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Regulatory Mutations

Regulatory mutations occur in non-coding regions of DNA that control gene expression rather than altering the protein-coding sequence itself. These mutations can affect how much or when a gene is expressed, potentially leading to phenotypic changes without changing the protein structure. In the context of the Dumbo mutation, if the mutation affects the regulation of a gene involved in ear size, it could lead to the observed large ears.

Protein-Coding Genes

Protein-coding genes are segments of DNA that contain the instructions for synthesizing proteins, which perform various functions in the organism. Mutations in these genes can lead to changes in the protein's structure and function, potentially resulting in observable traits. If the Dumbo mutation were a protein-coding mutation, it would imply a direct alteration in the protein responsible for ear development, rather than just a change in expression levels.

Phenotypic Expression

Phenotypic expression refers to the observable traits or characteristics of an organism, which result from the interaction of its genotype with the environment. In this case, the large ears of the Dumbo mouse represent a phenotypic change. Understanding whether this change arises from a regulatory mutation or a protein-coding mutation is crucial for determining the underlying genetic mechanisms responsible for the trait.

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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.

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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.

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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?

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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?

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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?

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Textbook Question

Thinking back to the discussion of gain-of-function and loss-of-function mutations, 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.

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Multiple Choice

What is the likely consequence when cells are unable to repair DNA damage caused by a mutagen?

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Multiple Choice

Which process helps to preserve the genetic information stored in DNA during DNA replication?

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