Ch. 14 - Gene Mutation, DNA Repair, and Transposition

Klug - Essentials of Genetics 10th Edition

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Klug 10th Edition

Ch. 14 - Gene Mutation, DNA Repair, and Transposition

Problem 20

Chapter 14, Problem 20

It is estimated that about 0.2 percent of human mutations are due to TE insertions, and a much higher degree of mutational damage is known to occur in some other organisms. In what way might a TE insertion contribute positively to evolution?

Verified step by step guidance

Understand what a Transposable Element (TE) insertion is: TEs are DNA sequences that can move around within the genome, sometimes inserting themselves into new locations.

Recognize that while TE insertions can disrupt genes and cause mutations, they can also create genetic diversity by introducing new sequences or regulatory elements.

Consider how TE insertions might provide raw material for evolution by creating new gene variants or altering gene expression patterns, potentially leading to beneficial traits.

Explore examples where TE insertions have been co-opted by the host genome to serve useful functions, such as creating new promoters, enhancers, or even new genes.

Conclude that TE insertions can contribute positively to evolution by increasing genetic variation and enabling novel adaptations that may be favored by natural selection.

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Key Concepts

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

Transposable Elements (TEs)

Transposable elements are DNA sequences that can move or copy themselves to new positions within the genome. They can disrupt gene function or regulation but also create genetic diversity by causing mutations, gene duplications, or rearrangements.

Mutations and Genetic Variation

Mutations are changes in the DNA sequence that can be harmful, neutral, or beneficial. Genetic variation arising from mutations, including TE insertions, provides raw material for natural selection and evolutionary adaptation.

Positive Evolutionary Impact of TE Insertions

TE insertions can contribute positively by creating new regulatory elements, altering gene expression, or generating novel genes. These changes can lead to advantageous traits that improve survival or reproduction, thus driving evolutionary innovation.

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What genetic defects result in the disorder xeroderma pigmentosum (XP) in humans? How do these defects create the phenotypes associated with the disorder?

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Compare DNA transposons and retrotransposons. What properties do they share?

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Textbook Question

In maize, a Ds or Ac transposon can alter the function of genes at or near the site of transposon insertion. It is possible for these elements to transpose away from their original insertion site, causing a reversion of the mutant phenotype. In some cases, however, even more severe phenotypes appear, due to events at or near the mutant allele. What might be happening to the transposon or the nearby gene to create more severe mutations?

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Textbook Question

In a bacterial culture in which all cells are unable to synthesize leucine (leu⁻), a potent mutagen is added, and the cells are allowed to undergo one round of replication. At that point, samples are taken, a series of dilutions are made, and the cells are plated on either minimal medium or minimal medium containing leucine. The first culture condition (minimal medium) allows the growth of only leu⁺ cells, while the second culture condition (minimal medium with leucine added) allows growth of all cells. The results of the experiment are as follows:

What is the rate of mutation at the locus associated with leucine biosynthesis?

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Textbook Question

Presented here are hypothetical findings from studies of heterokaryons formed from seven human xeroderma pigmentosum cell strains:

These data are measurements of the occurrence or nonoccurrence of unscheduled DNA synthesis in the fused heterokaryon. None of the strains alone shows any unscheduled DNA synthesis. Which strains fall into the same complementation groups? How many different groups are revealed based on these data? What can we conclude about the genetic basis of XP from these data?

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Textbook Question

Skin cancer carries a lifetime risk nearly equal to that of all other cancers combined. Following is a graph [modified from K. H. Kraemer (1997). Proc. Natl. Acad. Sci. (USA) 94:11 14] depicting the age of onset of skin cancers in patients with or without XP, where the cumulative percentage of skin cancer is plotted against age. The non-XP curve is based on 29,757 cancers surveyed by the National Cancer Institute, and the curve representing those with XP is based on 63 skin cancers from the Xeroderma Pigmentosum Registry.

Provide an overview of the information contained in the graph.

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