By John Brennan | Updated Aug 30, 2022
Gregor Mendel, the 19th‑century Austrian monk whose pea‑plant experiments laid the groundwork for modern genetics, discovered the basic principles of inheritance that still underpin genetics today. Yet not all traits follow Mendel’s simple rules – many are shaped by multiple genes, a phenomenon known as polygenic inheritance.
Mendelian traits arise from a single gene and are inherited in a predictable pattern. If both parents carry different versions (heterozygous), the offspring have a 3‑in‑4 chance of expressing the dominant allele and a 1‑in‑4 chance of expressing the recessive allele. If both parents are homozygous for the same allele, all children inherit that allele. When one parent is homozygous dominant and the other homozygous recessive, every child will be heterozygous.
Many monogenic disorders follow Mendelian inheritance. Cystic fibrosis, for instance, is caused by a recessive mutation in the CFTR gene. A child must inherit two copies of the defective allele—one from each parent—to develop the disease. The probability of affected offspring can therefore be calculated directly from the parents’ genotypes.
Polygenic traits are influenced by several genes, each contributing a small effect. Human eye color, skin pigmentation, and height are classic examples. The final phenotype results from the combined action of many alleles, producing a wide spectrum of outcomes rather than a single dominant or recessive form.
While each contributing gene follows Mendelian rules, the aggregate trait resists simple prediction. For instance, the diverse skin tones seen in humans arise from multiple genetic variants; parents with different allele combinations can produce offspring with a broad range of pigmentation.
