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Correct Answer: frameshift
**missense mutation**
a missense mutation is a type of genetic alteration where a single nucleotide change results in the substitution of one amino acid for another in the protein produced by a gene. while this type of mutation can affect the protein's function, in the scenario of insulin being reduced to 33 amino acids from its normal 51, a missense mutation alone does not typically result in a significant reduction in the length of the peptide chain. instead, it would alter specific amino acids, which might still impair function but not predominantly change the size of the insulin protein.
**frameshift mutation**
a frameshift mutation occurs due to insertions or deletions of a number of nucleotides in a dna sequence that is not divisible by three. since the genetic code is read in triplets (codons), this shifts the reading frame and alters the entire amino acid sequence downstream of the mutation. this type of mutation can lead to a drastically shortened protein, as seen in the insulin with only 33 amino acids. typically, a frameshift mutation introduces a premature stop codon, resulting in a truncated protein, which could explain the significant reduction in insulin size in the described case.
**point mutation**
a point mutation refers to a change in a single nucleotide in the dna sequence. although this can lead to a missense mutation or a nonsense mutation (where a codon is changed to a stop codon, leading to premature termination of the protein), a simple point mutation changing one amino acid would not account for the large decrease in insulin length from 51 to 33 amino acids. therefore, while a point mutation could contribute to functional loss if it results in a critical amino acid change or creates a stop codon, it is less likely to be responsible for such a drastic reduction in peptide length by itself.
**conclusion**
given that the person's insulin is significantly shorter, the most likely type of mutation responsible would be a frameshift mutation. this mutation would alter the reading frame of the insulin gene, potentially introducing a stop codon that prematurely ends the peptide chain. this results in a dysfunctional protein that is unable to effectively signal glucose uptake into cells, characteristic of the symptoms observed in type i diabetes mellitus. while other mutations can also lead to loss of function, the specific shortening of the insulin protein strongly points towards a frameshift mutation.
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