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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
All textbooksKlug 12th EditionCh. 15 - Gene Mutation, DNA Repair, and TranspositionProblem 25
Chapter 15, Problem 25

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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1
Identify the types of mutations: Begin by distinguishing between chromosomal mutations (such as deletions, duplications, inversions, and translocations) and gene mutations (such as point mutations, insertions, and deletions) that can result from high-energy radiation exposure.
Design a short-term study: Focus on immediate effects by collecting and analyzing somatic cell samples from survivors to identify chromosomal aberrations using techniques like karyotyping and fluorescence in situ hybridization (FISH).
Plan a long-term study: Investigate germ-line mutations by examining the offspring of survivors for inherited genetic changes. Use whole-genome sequencing to detect subtle gene mutations that may have been passed down.
Consider somatic tissue effects: Evaluate the impact of radiation on somatic tissues by assessing the incidence of cancer and other diseases in the exposed population, using epidemiological studies to track health outcomes over time.
Address germ-line tissue effects: Study the potential for radiation-induced mutations to affect future generations by analyzing reproductive health and genetic disorders in the descendants of those exposed to radiation.

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Key Concepts

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

Chromosomal Mutations

Chromosomal mutations involve changes in the structure or number of chromosomes, which can lead to significant genetic disorders or variations. These mutations can result from high-energy radiation causing breaks in DNA strands, leading to deletions, duplications, or translocations of chromosomal segments. Understanding these mutations is crucial for assessing the immediate and long-term impacts of radiation exposure on the population.
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Mutations and Phenotypes

Gene Mutations

Gene mutations are alterations in the nucleotide sequence of a gene, which can affect protein synthesis and function. High-energy radiation can induce point mutations, insertions, or deletions in the DNA sequence, potentially leading to diseases or phenotypic changes. Analyzing gene mutations helps in understanding the molecular basis of radiation effects on individuals and their descendants.
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Somatic vs. Germ-line Effects

Somatic mutations occur in non-reproductive cells and affect only the individual, while germ-line mutations occur in reproductive cells and can be passed to offspring. In studying radiation effects, it is essential to differentiate between these two types of mutations, as somatic mutations may lead to cancer or other health issues in survivors, whereas germ-line mutations can have hereditary implications for future generations.
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Related Practice
Textbook Question

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?

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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
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?
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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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