What is the difference between dominance and epistasis? Why didn't any dihybrid crosses studied by Mendel show epistasis?

To understand the difference, we need to know that both dominance and epistasis are related to how genes express themselves, but they work at different levels.

Dominance

Dominance happens between alleles of the same gene. In a pair of alleles (like Aa), the dominant allele masks or hides the effect of the recessive one. For example, in pea plants, tall (T) is dominant and dwarf (t) is recessive. So in genotype Tt, the plant will be tall, because the dominant T shows its effect and t remains hidden.

So, dominance is an interaction between two alleles of the same gene, present at the same locus (same position on homologous chromosomes).

Epistasis

Epistasis happens between alleles of different genes, located at different loci. In this, one gene can mask or modify the effect of another gene. The gene that does the masking is called the epistatic gene and the gene whose expression is affected is called the hypostatic gene.

For example, in Labrador dogs, one gene controls the pigment colour (black or brown), and another gene controls whether pigment is deposited in fur or not. Even if a dog has the gene for black or brown colour, if it has two recessive alleles (ee) at the second locus, no pigment is deposited and the dog will be yellow. So, the e gene is epistatic over the pigment gene.

So, epistasis is interaction between two different genes, where one gene changes or hides the effect of another gene.

Why Mendel's Dihybrid Crosses Did Not Show Epistasis?

Mendel studied seven different characters in pea plants like seed shape, seed colour, flower position, pod shape, etc. In all these characters, each trait was controlled by a single gene with clear dominant and recessive alleles and the genes were independent of each other, not interfering with each other's expression.

So, when he did dihybrid crosses, like round-yellow (RRYY) × wrinkled-green (rryy), the two genes for shape and colour acted independently. There was no gene masking another gene's expression. Hence, he always got the classic 9:3:3:1 phenotypic ratio, which is seen only when there is no epistasis.

Also, Mendel was very careful in choosing traits that were independent and clear in expression. Modern science now knows that many genes do show epistasis, but Mendel was lucky that his selected traits did not. If epistasis was present, the phenotypic ratios would have been different, like 12:3:1 or 9:7 or 13:3, etc.

So, Mendel's dihybrid crosses didn't show epistasis because he unknowingly selected traits controlled by independent and non-interacting genes.


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