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Question 8
Consider the template strand of a hypothetical gene, shown below. The exons are in bold type. 3' TAC AAA CCG GCC TTT GCC AAA CCC AAC CTA AAT ATG AAA ATT 5' Note: 1... show full transcript
Step 1
Answer
To determine the number of amino acids in the polypeptide, we need to identify the start and stop codons in the given DNA sequence. The start codon (TAC) translates into Methionine, which is the first amino acid. Next, we calculate the number of complete codons between the start codon and the stop codon.
The sequence is: 3' TAC AAA CCG GCC TTT GCC AAA CCC AAC CTA AAT ATG AAA ATT 5'
From the provided sequence, the relevant codons are:
The relevant stop codons from the sequence are ATC, ATT, or ACT. In this strand, we find the codons before the first stop codon. Counting them gives:
Thus, the total number of amino acids represented by the gene is 8.
Step 2
Answer
For the shorter polypeptide that consists of only five amino acids, one possible nucleotide change that could lead to truncation may involve the start or stop codon. By comparing the regular triplet read sequence with the mutation:
The normal sequence has ATG coding for Methionine, while a likely mutation could have changed 'AAT' to 'ATT' or 'ACT', which would have led to an earlier stop codon. This would effectively truncate the protein, resulting in a shorter polypeptide chain of five amino acids. Therefore, the nucleotide change is likely from AAT to ATT or ACT.
Step 3
Answer
The appearance of hereditary retinoblastoma in generations III and IV is indicative of an autosomal dominant trait, which signifies that only one copy of the mutated gene is sufficient for the trait to manifest.
By analyzing the pedigree, we can infer that the shaded male in generation III inherited the mutation from one of his parents. This mutation was either passed through to the offspring or arose independently in that generation, given the lack of prior history in generations I and II. In generation IV, any affected individuals must also have inherited the dominant trait from their parent in generation III, leading to the observed occurrences in this generation.
The nature of autosomal dominance can result in variable expressivity, meaning that affected individuals may show different phenotypic presentations, which could explain why not all heirs display the trait.
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