Among Betazoids in the world of Star Trek®, the ability to read minds is under the control of a gene called mindreader (abbreviated mr). Most Betazoids can read minds, but rare recessive mutations in the mr gene result in two alternative phenotypes: delayed-receivers and insensitives. Delayed-receivers have some mind-reading ability but perform the task much more slowly than normal Betazoids. Insensitives cannot read minds at all. Betazoid genes do not have introns, so the gene only contains coding DNA. It is 3332 nucleotides in length, and Betazoids use a four-letter genetic code.
The following table shows some data from five unrelated mr mutations.

For each mutation, provide a plausible explanation for why it gives rise to its associated phenotype and not to the other phenotype. For example, hypothesize why the mr-1 nonsense mutation in codon 829 gives rise to the milder delayed-receiver phenotype rather than the more severe insensitive phenotype. Then repeat this type of analysis for the other mutations. (More than one explanation is possible, so be creative within plausible bounds!)

Verified step by step guidance

1. Understand the genetic code and the impact of mutations: The mr gene is 3332 nucleotides long, and Betazoids use a four-letter genetic code. Each codon consists of three nucleotides, and mutations can alter the resulting protein's structure and function. The phenotypes (delayed-receiver and insensitive) are determined by the severity of the mutation's impact on the protein's function.
2. Analyze mr-1 (Nonsense mutation in codon 829): A nonsense mutation introduces a premature stop codon, truncating the protein. Since codon 829 is relatively late in the gene, the majority of the protein is still synthesized. This partial protein may retain some functionality, leading to the delayed-receiver phenotype rather than the complete loss of function seen in insensitives.
3. Analyze mr-2 (Missense mutation in codon 52): A missense mutation changes one amino acid in the protein. Since codon 52 is early in the gene, this mutation likely alters the protein's structure but does not completely disrupt its function. This partial functionality could explain the delayed-receiver phenotype.
4. Analyze mr-3 (Deletion of nucleotides 83–150): This deletion removes a segment of the gene, potentially causing a frameshift mutation. However, if the deletion does not disrupt critical functional domains of the protein, the resulting protein may still retain partial activity, leading to the delayed-receiver phenotype.
5. Analyze mr-4 and mr-5 (Missense mutation in codon 192 and deletion of nucleotides 83–93): The missense mutation in codon 192 likely disrupts a critical functional domain of the protein, leading to the insensitive phenotype. Similarly, the deletion of nucleotides 83–93 may cause a frameshift or remove essential amino acids, resulting in a complete loss of function and the insensitive phenotype.

Key Concepts

Gene Mutations

Gene mutations are alterations in the DNA sequence of a gene, which can affect the function of the protein produced. These mutations can be classified into several types, including nonsense mutations, which introduce a premature stop codon, and missense mutations, which result in a different amino acid being incorporated into the protein. Understanding how these mutations impact protein function is crucial for explaining the resulting phenotypes.

Phenotype Expression

Phenotype expression refers to the observable traits or characteristics of an organism, which result from the interaction of its genotype with the environment. In the context of the Betazoids, the phenotypes of delayed-receivers and insensitives arise from specific mutations in the mr gene. The severity of the phenotype often correlates with the type and extent of the mutation, influencing the protein's functionality.

Recessive vs. Dominant Traits

In genetics, traits can be classified as dominant or recessive based on their expression in the presence of alleles. Recessive traits, like the insensitivity phenotype in Betazoids, require two copies of the mutated allele to be expressed, while dominant traits can manifest with just one copy. This distinction is essential for understanding why certain mutations lead to milder or more severe phenotypes based on their genetic inheritance patterns.