Ch. 26 - Population and Evolutionary Genetics

Klug - Concepts of Genetics 12th Edition

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

Klug 12th Edition

Ch. 26 - Population and Evolutionary Genetics

Problem 30

Chapter 26, Problem 30

Shown below are two homologous lengths of the alpha and beta chains of human hemoglobin. Consult a genetic code dictionary, and determine how many amino acid substitutions may have occurred as a result of a single nucleotide substitution. For any that cannot occur as a result of a single change, determine the minimal mutational distance.
Alpha: ala val ala his val asp asp met pro
Beta: gly leu ala his leu asp asn leu lys

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First, write down the codons for each amino acid in the alpha and beta chains using the standard genetic code. For example, find the possible codons for 'ala' (alanine), 'val' (valine), 'his' (histidine), etc., for both chains.

Next, align the amino acids from the alpha and beta chains position by position to compare them directly: alpha (ala, val, ala, his, val, asp, asp, met, pro) versus beta (gly, leu, ala, his, leu, asp, asn, leu, lys).

For each pair of amino acids that differ, determine if one can be converted into the other by a single nucleotide substitution in the codon. To do this, compare all possible codons for the amino acid in the alpha chain with all possible codons for the amino acid in the beta chain and check if any pair differs by only one nucleotide.

If a single nucleotide substitution cannot explain the amino acid change, calculate the minimal mutational distance by counting the smallest number of nucleotide changes needed to convert one codon into another. This involves finding the codon pair with the fewest nucleotide differences.

Summarize the number of amino acid substitutions that can be explained by a single nucleotide change and list those that require more than one nucleotide substitution, specifying their minimal mutational distances.

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Key Concepts

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

Genetic Code and Codon-Amino Acid Relationship

The genetic code consists of nucleotide triplets called codons, each specifying a particular amino acid. Understanding how codons translate into amino acids is essential to determine how nucleotide changes affect protein sequences. A single nucleotide substitution can alter a codon, potentially changing the encoded amino acid or resulting in a synonymous mutation.

Single Nucleotide Substitution and Its Effects

A single nucleotide substitution changes one base in the DNA sequence, which can lead to a missense mutation if it alters the amino acid. Some amino acid changes require only one nucleotide change, while others need multiple substitutions. Identifying which amino acid differences arise from a single nucleotide change helps assess mutational impact.

Minimal Mutational Distance Between Codons

Minimal mutational distance refers to the smallest number of nucleotide changes needed to convert one codon into another. When amino acid substitutions cannot result from a single nucleotide change, calculating this distance helps understand the evolutionary or mutational steps required for the observed differences.

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Mutations and Phenotypes

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Textbook Question

A form of dwarfism known as Ellis–van Creveld syndrome was first discovered in the late 1930s, when Richard Ellis and Simon van Creveld shared a train compartment on the way to a pediatrics meeting. In the course of conversation, they discovered that they each had a patient with this syndrome. They published a description of the syndrome in 1940. Affected individuals have a short-limbed form of dwarfism and often have defects of the lips and teeth, and polydactyly (extra fingers). The largest pedigree for the condition was reported in an Old Order Amish population in eastern Pennsylvania by Victor McKusick and his colleagues (1964). In that community, about 5 per 1000 births are affected, and in the population of 8000, the observed frequency is 2 per 1000. All affected individuals have unaffected parents, and all affected cases can trace their ancestry to Samuel King and his wife, who arrived in the area in 1774. It is known that neither King nor his wife was affected with the disorder. There are no cases of the disorder in other Amish communities, such as those in Ohio or Indiana.

What is the most likely explanation for the high frequency of the disorder in the Pennsylvania Amish community and its absence in other Amish communities?

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Textbook Question

The original source of new alleles, upon which selection operates, is mutation, a random event that occurs without regard to selectional value in the organism. Although many model organisms have been used to study mutational events in populations, some investigators have developed abiotic molecular models. Soll et al. (2006. Genetics 175: 267-275) examined one such model to study the relationship between both deleterious and advantageous mutations and population size in a ligase molecule composed of RNA (a ribozyme). Soll found that the smaller the population of molecules, the more likely it was that not only deleterious mutations but also advantageous mutations would disappear. Why would population size influence the survival of both types of mutations (deleterious and advantageous) in populations?

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Textbook Question

A number of comparisons of nucleotide sequences among hominids and rodents indicate that inbreeding may have occurred more often in hominid than in rodent ancestry. Bakewell et al. (2007. Proc. Nat. Acad. Sci. [USA] 104: 7489-7494) suggest that an ancient population bottleneck that left approximately 10,000 humans might have caused early humans to have a greater chance of genetic disease. Why would a population bottleneck influence the frequency of genetic disease?

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Textbook Question

Recent reconstructions of evolutionary history are often dependent on assigning divergence in terms of changes in amino acid or nucleotide sequences. For example, a comparison of cytochrome c shows 10 amino acid differences between humans and dogs, 24 differences between humans and moths, and 38 differences between humans and yeast. Such data provide no information as to the absolute times of divergence for humans, dogs, moths, and yeast. How might one calibrate the molecular clock to an absolute time clock? What problems might one encounter in such a calibration?

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