Non-Mendelian Inheritance

Core Concept

Not every trait follows Mendel's simple dominant/recessive pattern. In non-Mendelian inheritance, alleles interact in more nuanced ways: some blend or both show at once, some genes affect many traits, some traits are controlled by many genes, and the environment can shift the outcome. These patterns extend rather than contradict Mendel — his laws of segregation and assortment still operate underneath.

Key Concepts

Incomplete dominance

In incomplete dominance, the heterozygote has an intermediate phenotype between the two homozygotes. A classic example is snapdragon flower color: red (CᴿCᴿ) × white (CᵂCᵂ) gives pink (CᴿCᵂ). Neither allele is fully dominant; each contributes a partial "dose." Note the genotypic and phenotypic ratios coincide (1:2:1) — a clue that dominance is incomplete.

Codominance

In codominance, the heterozygote expresses both alleles fully and simultaneously — neither masks the other. The human ABO blood group is the model: the Iᴬ and Iᴮ alleles are codominant, so an IᴬIᴮ person has type AB blood, expressing both A and B antigens. (A and B are each dominant over the i allele, which produces neither antigen, giving type O.)

Multiple alleles

A gene can have more than two alleles in a population, even though any single individual carries only two. The ABO gene has three common alleles — Iᴬ, Iᴮ, and i — producing four phenotypes (A, B, AB, O). Multiple alleles increase the number of possible genotypes and phenotypes without violating segregation.

Pleiotropy

Pleiotropy occurs when one gene influences multiple, seemingly unrelated traits. Many genetic disorders are pleiotropic: a single mutated gene can affect several systems. For example, mutations in the gene for fibrillin (Marfan syndrome) affect the skeleton, eyes, and heart; sickle-cell mutations affect red cells, and secondarily many organs.

Epistasis

Epistasis is when the alleles of one gene mask or modify the expression of another gene. A well-known example is coat color in Labrador retrievers: one gene (B) determines black vs. brown pigment, but a separate gene (E) must be functional for any pigment to be deposited — an ee dog is yellow regardless of its B genotype. Epistasis changes Mendelian ratios (e.g., a dihybrid cross giving 9:3:4 instead of 9:3:3:1).

Polygenic inheritance

Polygenic traits are controlled by many genes, each contributing a small additive effect. The result is continuous variation — a bell-shaped distribution of phenotypes. Human height, skin color, and weight are polygenic. More contributing genes mean smoother, more continuous variation and many intermediate phenotypes.

Environment and phenotype

Phenotype = genotype + environment. The same genotype can produce different phenotypes in different environments: a plant's height depends on water, light, and soil; human height depends partly on nutrition; and conditions like phenylketonuria (PKU) — severe with a normal diet, largely harmless with a special low-phenylalanine diet — show that environmental intervention can reshape an otherwise "genetic" outcome. Norm of reaction describes the range of phenotypes a genotype can produce across environments.

How It Works

The underlying mechanism is still segregation and assortment at the DNA level; what differs is how the gene products interact to build a phenotype. Incomplete dominance and codominance reflect how much product each allele makes (a half-dose vs. two full doses). Epistasis reflects genes acting in the same biochemical pathway (if an early step fails, later genes don't matter). Polygenic traits reflect many genes summing together with environmental noise. In every case, the alleles segregate normally in meiosis — only the mapping from genotype to phenotype changes.

How it works

The underlying mechanism is still segregation and assortment at the DNA level; what differs is how the gene products interact to build a phenotype. Incomplete dominance and codominance reflect how much product each allele makes (a half-dose vs. two full doses). Epistasis reflects genes acting in the same biochemical pathway (if an early step fails, later genes don't matter). Polygenic traits reflect many genes summing together with environmental noise. In every case, the alleles segregate normally in meiosis — only the mapping from genotype to phenotype changes.

Common confusions

• "Incomplete dominance and codominance are the same." Wrong — incomplete dominance blends (pink, intermediate); codominance shows both fully at once (AB).
• "Dominant alleles are always more common." Wrong — the i (type O) allele is recessive yet the most common ABO allele in many populations.
• "Polygenic means 'many traits from one gene.'" Wrong — that is pleiotropy (one gene → many traits). Polygenic is many genes → one trait.
• "Epistasis is just dominance within one gene." Wrong — dominance is between alleles of the same gene; epistasis is between alleles of different genes.
• "Environment only affects plants." Wrong — environment shapes human phenotypes too (nutrition and height, diet and PKU).

Quick review

• Incomplete dominance → intermediate heterozygote (1:2:1 ratio).
• Codominance → both alleles shown (AB blood).
• Multiple alleles → ABO system (Iᴬ, Iᴮ, i).
• Pleiotropy → one gene affects many traits.
• Epistasis → one gene masks another (9:3:4).
• Polygenic → many genes, continuous variation.
• Environment modifies phenotype; norm of reaction = range of outcomes.
• All still follow segregation/assortment at the DNA level.