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You are working with a newly discovered mutagen, and you wish to determine the base change that it introduces into DNA. Thus far, you have determined that the mutagen chemically alters a single base in such a way that its base- pairing properties are altered permanently. To determine the specificity of the alteration, you examine the amino acid changes that take place after mutagenesis. A sample of what you find is shown here: \(\begin{array}{cl}\text { Original: } & \text { Gln-His-Ile-Glu-Lys } \\\ \text { Mutant: } & \text { Gln-His-Met-Glu-Lys } \\ \text { Original: } & \text { Ala-Val-Asn-Arg } \\ \text { Mutant: } & \text { Ala-Val-Ser-Arg } \\\ \text { Original: } & \text { Arg-Ser-Leu } \\ \text { Mutant: } & \text { Arg-Ser-Leu-Trp-Lys-Thr-Phe }\end{array}\) What is the base-change specificity of the mutagen?

Short Answer

Expert verified
The mutagen changes cytosine (C) to guanine (G).

Step by step solution

01

Identify Changed Amino Acids

Examine the changes in the amino acid sequences caused by the mutagen. In the first sequence, Ile (Isoleucine) is changed to Met (Methionine). In the second sequence, Asn (Asparagine) is changed to Ser (Serine). In the third sequence, additional amino acids Trp (Tryptophan), Lys (Lysine), Thr (Threonine), and Phe (Phenylalanine) are introduced after Leu (Leucine).
02

Codon Analysis for Changed Amino Acids

Determine the codons for the original and mutant amino acids. Ile's codons are AUU, AUC, AUA, and Met's codon is AUG. Asn's codons are AAU, AAC, and Ser's possible replacement is UCU, UCC, UCA, UCG, AGU, AGC. Note that the appearance of extra amino acids can be due to a stop codon being replaced (e.g., UGA).
03

Base Pair Consideration

Examine how a single base change could account for these amino acid changes. For the Ile to Met conversion, a change could occur from AUA to AUG (A changes to G). For Asn to Ser, consider the change from AAC to AGC (C changes to G). In the third sequence, a stop codon like UGA could be changed to UGG (Trp), followed by continued translation since other stop codons were no longer functional.
04

Determine Base Change Specificity

Based on the codon changes, identify the specific base change caused by the mutagen. The mutagen appears to change the nucleotide cytosine (C) to guanine (G). This aligns with the observed amino acid changes in all sequences.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Base Pair Alteration
Base pair alteration involves the modification of the standard pairing between nucleotides in DNA. This change often happens due to the action of a mutagen, a chemical or agent that causes mutations in the DNA sequence. Upon alteration, these base pairs no longer interact in the standard adenine-thymine or cytosine-guanine pairings.

The impact of a base pair alteration is significant because it permanently changes the DNA sequence's properties. In the context of our exercise, the alteration is specific, changing cytosine (C) into guanine (G). This results in varied protein synthesis outcomes since the DNA's template for RNA differs in its base sequence. This alteration shifts the genetic encoded information, leading to changes in the resulting amino acids during protein synthesis.
Amino Acid Sequence Analysis
Analyzing amino acid sequences is crucial in understanding the implications of genetic mutations. Sequencing provides insight into how proteins' structures and functions can change after a mutation. By comparing the original and mutant sequences, researchers can pinpoint which specific amino acids have been altered.

In our exercise, sequence comparisons reveal amino acid changes due to a base pair alteration. For example, an Isoleucine is switched to Methionine, and Asparagine is switched to Serine. These changes offer clues to the sort of mutations happening at the DNA level. The introduction of additional amino acids, such as Tryptophan and Lysine, suggests a disruption of normal termination processes. This could occur if a stop codon has been altered into coding for an amino acid instead, causing translations to continue unexpectedly.
Codon Changes
Codons are sequences of three nucleotides in RNA that correspond to specific amino acids or signal the end of protein synthesis. Mutations altering codons are significant because even a single nucleotide change can produce different amino acids.

In this context, analyze the shift from original to mutant codons. For instance, methionine (Met) replaces isoleucine (Ile) due to a change from the codon AUA to AUG. Similarly, serine (Ser) replaces asparagine (Asn) when AAC changes to AGC. These specific changes suggest that a cytosine has transformed into a guanine.

Additionally, heterogeneity in the length of the amino acid sequences, with added sequences in some mutants, hints at codon alterations that extend or modify protein synthesis. Such insights are critical for understanding how mutagens can significantly impact biological functions.

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Most popular questions from this chapter

a. Acridine orange is an effective mutagen for producing null alleles by mutation. Why does it produce null alleles? b. A certain acridine-like compound generates only single insertions. A mutation induced with this compound is treated with the same compound, and some revertants are produced. How is this outcome possible?

You are using nitrosoguanidine to "revert" mutant nic-2 (nicotinamide- requiring) alleles in Neurospora. You treat cells, plate them on a medium without nicotinamide, and look for prototrophic colonies. You obtain the following results for two mutant alleles. Explain these results at the molecular level, and indicate how you would test your hypotheses. a. With nic-2 allele 1, you obtain no prototrophs at all. b. With nic-2 allele \(2,\) you obtain three prototrophic colonies \(A, B,\) and \(C,\) and you cross each separately with a wild-type strain. From the cross prototroph \(\mathrm{A} \times\) wild type, you obtain 100 progeny, all of which are prototrophic. From the cross prototroph \(\mathrm{B} \times\) wild type, you obtain 100 progeny, of which 78 are prototrophic and 22 are nicotinamide requiring. From the cross prototroph \(\mathrm{C} \times\) wild type, you obtain 1000 progeny, of which 996 are prototrophic and 4 are nicotinamide requiring.

In adult cells that have stopped dividing, what types of repair systems are possible?

Why are many chemicals that test positive by the Ames test also classified as carcinogens?

Under what circumstances could nonhomologous end joining be said to be error prone?

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