In Labrador retrievers, coat color is determined by two genes. The B gene controls pigment color (B = black, b = brown), while the E gene controls pigment deposition. If a dog is homozygous recessive for the E gene (ee), the coat is yellow regardless of the B gene's alleles. What is the genetic phenomenon described here?

Core Concept

PILLAR 1 — MOLECULAR/CONCEPTUAL MECHANISM

Step-by-Step Analysis

In Labrador retrievers, coat color determination involves a biochemical cascade that synthesizes and deposits melanin pigments into hair shafts during follicular development. The B gene encodes a protein that modulates the enzymatic activity of tyrosinase—the rate-limiting enzyme that catalyzes the hydroxylation of tyrosine to L-DOPA and its subsequent oxidation to dopaquinone within melanosome organelles of melanocytes. When functional B allele products are present, dopaquinone is converted into eumelanin, producing dark pigmentation. The recessive b allele yields an altered protein with reduced binding affinity for tyrosinase substrates, shifting melanin synthesis toward a brown eumelanin variant.

Why Other Options Are Wrong

The E gene operates at a different regulatory level entirely—it encodes a receptor protein embedded in the melanocyte membrane that responds to melanocyte-stimulating hormone (MSH). When MSH binds this receptor, it triggers a G-protein coupled signaling cascade involving adenylate cyclase, elevated intracellular cyclic AMP (cAMP), and subsequent activation of protein kinase A. This phosphorylation cascade ultimately upregulates tyrosinase transcription and melanosome maturation, enabling mature melanin granules to be transferred to keratinocytes in the growing hair shaft. Homozygous recessive (ee) individuals produce a non-functional receptor with a mutated ligand-binding domain. Without MSH signal transduction, the downstream cAMP amplification never occurs, tyrosinase remains transcriptionally silent, and melanosomes fail to fully mature. Consequently, no melanin deposition transpires in the hair regardless of what functional B gene products exist in the cytoplasm. The coat appears yellow because the structural properties of unpigmented keratin reflect light in the yellow wavelength spectrum.

PILLAR 2 — STEP-BY-STEP LOGIC

The question asks us to identify the genetic phenomenon wherein the E gene genotype determines whether the B gene can be phenotypically expressed. This describes epistasis—a non-allelic gene interaction in which one locus (the epistatic gene) masks or completely suppresses the phenotypic expression of alleles at a second locus (the hypostatic gene). The ee genotype is epistatic to the B locus because the homozygous recessive condition at E eliminates the receptor-mediated signaling required for melanin synthesis, functionally silencing the B gene's contribution to the phenotype. The B gene is hypostatic because its alleles can only manifest when at least one dominant E allele produces a functional receptor.

This is specifically classified as recessive epistasis, which produces a characteristic 9:3:4 phenotypic ratio in F2 dihybrid crosses. The mechanism differs fundamentally from allelic interactions at a single locus—the masking occurs because the epistatic gene controls an upstream prerequisite step in a metabolic pathway. The E gene regulates whether the biochemical factory (the melanosome with its signaling apparatus) is operational, while the B gene determines the product specifications (black versus brown melanin) only after that factory is running.

PILLAR 3 — DISTRACTOR ANALYSIS

Option A, codominance, is a common trap because students recognize that two genes are interacting. However, codominance specifically describes a scenario at a single locus where both alleles are simultaneously expressed in the heterozygote (such as the ABO blood group, where both IA and IB antigens appear on erythrocyte membranes). The Labrador scenario involves complete masking across two separate loci, not shared expression of co-dominant alleles.

Option C, incomplete dominance, tempts students because heterozygous phenotypes appear intermediate. This phenomenon involves allele dosage effects at one gene, where the heterozygote produces approximately half the functional protein of the homozygous dominant, yielding a blended phenotype. Labrador coat color involves complete suppression of one gene's output by another gene's genotype—no intermediate blending of black, brown, and yellow occurs.

Option D, polygenic inheritance, attracts students who notice that coat color involves multiple genes. Polygenic inheritance describes additive effects of alleles at multiple loci contributing quantitatively to a single phenotypic trait along a continuous spectrum (like human height or skin pigmentation controlled by dozens of SNPs). The Labrador system involves discrete categorical outcomes and a hierarchical masking relationship, not additive quantitative accumulation of pigments from multiple contributing loci.