The Molecular Basis of Epistasis PART 2

In this article, we will go over the following kinds of epistasis: duplicate dominant, duplicate recessive, and polymeric inheritance. For the first three kinds, please refer back to my previous article.

Note: in the images below, pretend the boxes are filled with the letters of a dihybrid cross. Here they are for your reference:

Okay, let's get to it!

4) Duplicate Dominant

15:1

Both gene A and gene B code for the same phenotype, so in order to have the phenotype, the organism needs either a dominant A or dominant B gene. Here's what that looks like:

The A gene codes for a yellow product, and the B gene does too. So when either one (or both) is/are present, the green precursor is converted into a yellow product. When neither are present (aabb), it is converted to green. 

5) Duplicate Recessive (Complementary)

9:7

Dominants in both the gene A and gene B loci are needed to express the phenotype. This works in a sequential pathway, as depicted below:

Both the A and B genes are needed to convert the orange product into a yellow one. Obviously, the order could have been reversed, where B is the first enzyme and A is the second. But the concept remains the same, regardless.

Duplicate recessive epistasis is also called "complementary" because one gene complements the other (both are needed to create the phenotype). Compare this to recessive (supplementary) epistasis, covered in the last article. Here's a table comparing complementary and supplementary gene interaction:

6) Polymeric Interaction / Additive Gene Effect

9:6:1

Both gene A and gene B's products have the same effect when separate. However, when both are present, the result is a stronger (additive) phenotype. 

(the pathway could be either way)

In this case, having either A or B converted white to light brown product, while having both A and B gave two equivalents of brown, which created a darker color. 

So yeah, that's epistasis. Here's some resources to learn more about it:

Previous
Previous

Understanding Cancer's POV - The Tumor Microenvironment

Next
Next

The Molecular Basis of Epistasis PART 1