A geneticist is studying the inheritance of a trait in yeast. She observes that the offspring of two parents who are homozygous dominant (CC) have a 75% chance of expressing the trait. Which of the following is the most likely genotype of the non-expressing offspring?

Core Concept

PILLAR 1 — MOLECULAR/CONCEPTUAL MECHANISM

Step-by-Step Analysis

The correspondence between genotype and phenotype rests on molecular processes of transcription, translation, and protein function operating within the cell. A dominant allele (C) encodes a functional polypeptide—frequently an enzyme such as tryptophan synthase or a transcription factor like GAL4 in Saccharomyces cerevisiae—that drives the biochemical pathway producing the observable trait. When two copies of the functional allele are present (CC), the locus yields roughly double the mature mRNA transcripts compared to a single-copy state, and ribosomal translation in the cytoplasm generates proportionally more functional protein. However, dominance is not an intrinsic property of an allele; it emerges from the quantitative relationship between protein concentration and phenotypic threshold. Haploinsufficiency describes the condition in which one functional allele cannot sustain adequate protein levels to cross the activation threshold for downstream effectors. Genes encoding rate-limiting enzymes or dosage-sensitive transcription regulators—such as the yeast transcription factor GAL4, which must bind upstream activating sequences (UAS) at specific promoter sites to recruit RNA polymerase II—are especially vulnerable to dosage effects. When GAL4 concentration drops below the threshold needed to saturate its UAS binding sites, target genes like GAL1 and GAL10 fail to activate, and the cell cannot metabolize galactose. Similarly, a Cc heterozygote at a dosage-sensitive locus may produce insufficient protein to trigger the phenotypic pathway, effectively behaving as a non-expressing genotype despite retaining one dominant allele. Incomplete penetrance in heterozygotes can arise from stochastic variation in chromatin accessibility, histone acetylation patterns at the promoter, or micro-environmental fluctuations in metabolite concentrations that shift the probability of the transcriptional machinery successfully initiating gene expression.

Why Other Options Are Wrong

PILLAR 2 — STEP-BY-STEP LOGIC

The stimulus specifies that two parents described as homozygous dominant (CC) produce offspring with only a 75% probability of expressing the trait. Under strict Mendelian expectations, a CC × CC cross generates exclusively CC zygotes—each inheriting one C-bearing chromosome from each parent's homologous pair during meiosis—and every offspring should express the dominant phenotype at 100% frequency. The observed 25% non-expression among offspring of two parents displaying the dominant phenotype signals that a standard complete-dominance model fails here. Consider the possibility that one parent is actually Cc rather than CC, despite appearing phenotypically dominant. A CC × Cc mating produces offspring in a 1:1 ratio—50% CC and 50% Cc. If the C allele exhibits haploinsufficiency or incomplete penetrance such that roughly half of Cc individuals fail to express the trait, then the expected proportion of expressing offspring becomes: all CC individuals (50% of total) plus half of Cc individuals (25% of total), yielding 75% expression. The remaining 25% of offspring are Cc individuals who, owing to insufficient gene product falling below the phenotypic threshold, constitute the non-expressing class. This quantitative fit between the predicted 75% and the observed 75% expression rate identifies Cc as the most probable genotype of the non-expressing offspring. The reasoning requires integrating knowledge of meiotic chromosome segregation—where each gamete receives one allele from the parent's diploid complement—with the concept that protein dosage, not mere allele identity, determines phenotypic output at sensitive loci.

PILLAR 3 — DISTRACTOR ANALYSIS

Option A (CC) ensnares students who attribute the 25% non-expression to purely environmental suppression of an otherwise intact CC genotype. The structural flaw is that CC individuals produce protein from both alleles; even under moderate environmental stress, the dual-copy dosage buffer typically sustains expression above threshold. Invoking environment alone ignores the genetic architecture that a 75:25 ratio mirrors the progeny proportions expected from a cross involving heterozygosity, pointing to a genotypic—not merely external—explanation.

Option C (cc) attracts students who recognize the classic Mendelian 3:1 phenotypic ratio from a dihybrid or monohybrid heterozygote cross (Cc × Cc) and reflexively assign the homozygous recessive genotype to the non-expressing quarter. This constitutes a pattern-matching error: the question explicitly states that both parents are homozygous dominant. Producing a cc offspring from two CC parents would demand simultaneous de novo mutations inactivating both C alleles within a single meiotic event—a compound probability on the order of 10⁻¹² per nucleotide per generation, rendering cc astronomically less probable than a single-allele conversion yielding Cc.

Option D ("It cannot be determined") captures students who detect the tension between the stated parental genotype (CC) and the non-Mendelian offspring ratio but conclude the data are insufficient for resolution. This reflects incomplete mastery of non-Mendelian inheritance mechanisms—specifically haploinsufficiency and incomplete penetrance—that provide coherent explanatory frameworks. The 75% expression figure is a precise quantitative constraint that, combined with dosage-sensitivity principles, permits a definitive genotype assignment for the non-expressing class.