Ch. 15 - Gene Mutation, DNA Repair, and Transposition

Klug - Concepts of Genetics 12th Edition

Klug12th EditionConcepts of Genetics ISBN: 9780135564776Not the one you use?Change textbook

Klug 12th Edition

Ch. 15 - Gene Mutation, DNA Repair, and Transposition

Problem 26

Chapter 15, Problem 26

With the knowledge that radiation causes mutations, many assume that human-made forms of radiation are the major contributors to the mutational load in humans. What evidence suggests otherwise?

Verified step by step guidance

Step 1: Understand the types of radiation. Natural sources of radiation include cosmic rays, radon gas, and terrestrial sources, while human-made sources include medical X-rays, nuclear power plants, and nuclear weapons.

Step 2: Consider the exposure levels. Natural sources of radiation are ubiquitous and contribute to a constant low-level exposure, whereas human-made sources are typically more localized and controlled.

Step 3: Examine the contribution of natural radiation. Studies have shown that natural background radiation accounts for a significant portion of the radiation exposure humans receive, suggesting it plays a major role in the mutational load.

Step 4: Review scientific studies. Research comparing mutation rates in populations exposed to different levels of natural and human-made radiation can provide insights into the relative contributions of each source.

Step 5: Analyze the impact of lifestyle and environment. Factors such as altitude, geographic location, and building materials can influence exposure to natural radiation, further supporting its significant role in mutational load.

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Key Concepts

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

Natural Background Radiation

Natural background radiation is the ionizing radiation that is present in the environment, originating from cosmic rays, radon gas, and terrestrial sources. This type of radiation contributes significantly to the overall radiation exposure in humans, often exceeding that from human-made sources. Understanding the levels and effects of natural background radiation is crucial for evaluating its role in mutation rates.

Mutation Rate and Sources

The mutation rate refers to the frequency at which mutations occur in a given gene or organism over time. While radiation can induce mutations, other factors such as chemical exposure, biological processes, and replication errors also contribute to the overall mutational load. Analyzing the relative contributions of these various sources helps clarify the impact of human-made radiation on mutation rates.

Epidemiological Studies

Epidemiological studies investigate the patterns, causes, and effects of health and disease conditions in defined populations. These studies can provide evidence regarding the relationship between radiation exposure and mutation rates by comparing populations with different levels of exposure. Such research is essential for understanding whether human-made radiation significantly contributes to the mutational load compared to natural sources.

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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

Imagine yourself as one of the team of geneticists who launches a study of the genetic effects of high-energy radiation on the surviving Japanese population immediately following the atom bomb attacks at Hiroshima and Nagasaki in 1945. Demonstrate your insights into both chromosomal and gene mutation by outlining a short-term and long-term study that addresses these radiation effects. Be sure to include strategies for considering the effects on both somatic and germ-line tissues.

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Textbook Question

What evidence indicates that mutations in human DNA mismatch repair genes are related to certain forms of cancer?

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Textbook Question

Among Betazoids in the world of Star Trek®, the ability to read minds is under the control of a gene called mindreader (abbreviated mr). Most Betazoids can read minds, but rare recessive mutations in the mr gene result in two alternative phenotypes: delayed-receivers and insensitives. Delayed-receivers have some mind-reading ability but perform the task much more slowly than normal Betazoids. Insensitives cannot read minds at all. Betazoid genes do not have introns, so the gene only contains coding DNA. It is 3332 nucleotides in length, and Betazoids use a four-letter genetic code.

The following table shows some data from five unrelated mr mutations.

For each mutation, provide a plausible explanation for why it gives rise to its associated phenotype and not to the other phenotype. For example, hypothesize why the mr-1 nonsense mutation in codon 829 gives rise to the milder delayed-receiver phenotype rather than the more severe insensitive phenotype. Then repeat this type of analysis for the other mutations. (More than one explanation is possible, so be creative within plausible bounds!)

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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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