The question states that the individual with three sex chromosomes has a condition called polysomy. Recall that a normal individual will only carry two copies of a chromosome.

This abnormality occurs when meiosis isn’t carried out properly. A daughter cell from meiosis can contain an extra chromosome if sister chromatids don’t separate properly during anaphase II (a process called nondisjunction). This extra chromosome can be carried over to the offspring, giving rise to a polysomic individual.

Fertilization of two sperm cells with two eggs gives rise to fraternal twins (non-identical twins) and splitting of a single fertilized egg into two or more eggs gives rise to monozygotic twins (identical twins); therefore, you can eliminate these two answer choices. After meiosis, females always possess multiple polar bodies. During meiosis in females, most of the cellular content is transferred to a single daughter cell: the egg. The remaining daughter cells contain the remnants and are called polar bodies. These polar bodies don’t participate in development and fertilization.

This question is asking about the phase of Meiosis, during which disjunction (separation) of chromosomes normally occurs. While Metaphase can sometimes be a seductive answer, note that disjunction officially occurs during Anaphase.

This mutation replaced UAU (a coding codon) with UAG (a stop codon). The most descriptive term for this kind of replacement is a nonsense mutation.

Note that an easy way to remember the stop codons is UGA ("u" get away), UAA ("u" are away), and UAG ("u" are gone).

A nonsense mutation results in premature addition of a stop codon. A missense mutation is a point mutation that results in a different codon, which ultimately codes for a different amino acid in the polypetide sequence. A frameshift mutation results from and insertion or deletion of a nucleotide, resulting in a change in the reading frame. Frameshift mutations often indirectly result in nonsense mutations, but are not the best answer choice given.

Whenever a base pair is replaced by another base pair in the DNA double helix, it is referred to as a point mutation. If the amino acid is not changed by the mutation, we can refer to the mutation as a silent mutation, as the primary protein structure is not affected.

Point mutation: CATGA becomes CAGGA

Insertion mutations occur when additional bases are inserted into the DNA sequence.

Insertion mutation: CATGA becomes CATACTGA

Frameshift mutations can result from insertions or deletions when the number of nucleotides added/removed is not a multiple of three. Since codons are grouped by threes, any change that is not a multiple of three will alter the grouping of every codon downstream of the mutation, severly altering the primary protein structure.

Frameshift mutation: CATGA becomes CAATGA

A nonsense mutation results in a premature stop codon, and early translation termination. This can arise from a frameshift mutation, point mutation, insertion, or deletion.

Nonsense mutation: CATGA becomesCATTTAGA (When transcribed, this sequence becomes the mRNA UCUAAAUG, where UAA is a stop codon).

The trait is recessive because affected individuals do not occur in every generation. Additionally, dominant traits do not result in "carriers". Individuals are either affected or unaffected.

The best answer is a nonsense mutation, which is defined as a point mutation that gives rise to an early stop codon, thus truncating any protein products prematurely. These are typically devastating mutations for protein function.

The beta cell-specific Dia mutation in group C causes results similar to the global Dia mutation in group B. From this, we can conclude that Dia is functioning within the beta cells. Essentially, deleting Dia from the beta-cells is equivalent to deleting it from the entire body. Additionally, loss of Dia in skeletal muscle in group D seems to have no phenotypic effect, indicating that Dia is not necessary in skeletal muscle.

Pancreatic beta cells are responsible for insulin production, while skeletal muscle plays a significant role in insulin sensitivity. Since loss of Dia in beta cells leads to high blood glucose, we can conclude that the role of Dia is in the promoting the production of insulin, and that the gene plays no role in insulin sensitivity.

The question informs us that the mutational defect in the gene involves the enzyme's ability to load copper onto apoceruloplasmin. Healthy individuals are able to load copper to apoceruloplasmin, creating serum-soluble ceruloplasmin. With this process disrupted in an individual with Wilson's Disease, we would expect that less ceruloplasmin would be produced because copper could not be transported. We would expect to see reduced serum levels of the complete protein, and high levels of copper building up in hepatocytes and circulatory serum.

Recessive alleles are often created by mutated versions of functional genes that encode broken/nonfunctional proteins. The question is thus asking us which of the mutations is likely to result in a nonfunctional or abnormal protein.

Silent mutations are types of mutations that result in the insertion of the same amino acid due to the degeneracy of the genetic code and, therefore, will not cause any noticeable change in the protein. Essentially, even organisms with the mutation will still show the dominant allele.

Frameshift mutations change the reading frame used for translation and oftentimes result in premature stop codons. Nonsense mutations are mutations that specifically result in premature stop codons and generally result in nonfunctional proteins. Missense mutations lead to the insertion of a different amino acid at the normal site. This can lead to serious problems for the functionality of the protein, particularly if the mutation is present in the active site or another area that is highly conserved throughout evolution.