HomeArticlesIncomplete Dominance, Codominance, Polygenic Traits, and Epistasis!
Incomplete Dominance, Codominance, Polygenic Traits, and Epistasis!
October 19, 2019
Captioning is on! To turn off, click the CC button at bottom right. Follow the amoebas on Twitter (@amoebasisters) and Facebook! What do snapdragons, human height, and speckled
chickens have in common? Well they are easily identified as non-Mendelian traits. By non-Mendelian,
we mean that, genetically, they are RULE BREAKERS! They don’t follow the regular Mendelian
rule that having a dominant allele means the dominant trait will show. Remember in our
guinea pig video, having a dominant allele—represented by a capital H—meant the guinea pig had
hair? Only if there was no dominant present, a genotype of hh, would there be a hairless
guinea pig? That’s a Mendelian trait. But what we’re going to cover is when these
traits are non-Mendelian and don’t follow those basic rules. Let’s first start by
snapdragons. We confess that when we heard this word, we thought they were some really
amazing kind of creature. Well they are amazing but they’re flowers. So…I don’t know…that’s
not exactly what we envisioned. In snapdragon genetics, there can be 3 phenotypes. Red.
White. Or something in between—PINK! It’s called incomplete dominance. In incomplete
dominance, the dominant allele is not completely expressed with the recessive allele is around.
So if you cross a red flower (written RR) and a white flower (written rr), you get babies
that are Rr. But unlike a Mendelian trait, if incomplete dominance, that R allele is
not completely expressed when the r is around. So Rr in this case is pink! If you cross two
pink flowers (Rr), like shown in this Punnett square here…you can get offspring that are
red, white, or pink.Incomplete dominance is different from codominance. Codominance—like
a coworker—that pre-fix “co” should make you think together. They work together.
The alleles, that is. For that reason, we like to use different letters entirely. In
some breeds of chickens, there is a codominance involving color. Take a look at this Punnett
square. If you cross a black chicken—represented by BB—-and a white chicken—-represented
by WW——all the offspring here are BW. BW chickens are both black and white. Speckled!
See, both traits show up—this is the essence of codominance. And you know, what’s more
awesome than a speckled chicken? Well except for those silkie bantam chickens….By the
way, you will find that many people use different formatting for incomplete dominance and codominance.
Some people like to use different letters entirely for incomplete dominance—some people
don’t. Some people also prefer to do exponents with codominance—-some people don’t. Formatting
aside when solving Punnett squares, since we find this can really vary classroom to
classroom, the real concept is that in incomplete dominance—one allele is not completely dominant
over the other so you see an almost “in between” phenotype. If codominance, neither
allele is dominant over the other, so both alleles are expressed.Height is fascinating.
In our immediate family, Pinky is taller than Petunia. Our mom is also taller than Petunia.
How does this happen? There isn’t just one height gene. There’s LOTS of genes that
determine your height. What I mean by that is that you don’t just have a pair of alleles,
like AA, Aa, or aa that code for your height. It’s more like someone having a genotype
of AABbCcDD etc to ultimately determine height. And you inherit one allele for each of the
height genes—from each parent. All of those genes work together to determine your height.
Your skin color is also determined by many genes just like your height. These are called
polygenic traits. Poly means many—so “many” genes coding for one trait is what polygenic
means. By the way, both height and skin color can be influenced by environmental factors
as well. Nutrition growing up can affect your height just as spending a lot of time in the
sun can affect your skin color. However, this doesn’t change the genetics for this trait.And
finally, one more that we want to talk about, epistasis. Epistasis is when one gene really
depends on another gene for it to be expressed. I mean, it REALLY depends on this other gene.
So let’s pick an animal like a…. Ok…a….llama. Let’s say that this llama has a dominant
B allele which means its wool will be black. So BB or Bb means it will have black wool
and let’s say that if a llama has a pair of recessive alleles—bb—it will have brown
wool. Now what if there is another gene—an epistatic gene—that controls whether the
pigment will even be expressed in the llama wool in the first place? A llama can have
a genotype of CC, Cc, or cc for this epistatic gene. However, if a llama has the genotype
cc, it will not allow the other gene for wool color to even be expressed.Since we have two
genes here—the gene for wool color and the epistatic gene—- this calls for our favorite
16 square dihybrid. If you notice in this dihybrid crossing two heterozygote llamas
(BbCc and BbCc), BB and Bb will typically give a black llama and bb will typically give
a brown llama in all cases UNLESS the epistatic gene inherited is cc. If the llama has a cc
in its genotype, then the gene for wool color is not expressed and the llama is albino.
This means that no pigment is expressed at all. Pretty interesting. There are many other
non-Mendelian traits—we have another video on multiple alleles and a video on sex-linked
traits—which are also non-Mendelian. It’s kind of fascinating to see what can happen
with these rule breakers. One last thing. Keep in mind that when problem solving in
genetics, you do not want to just assume it’s non-Mendelian unless you are provided information
or clues in the problem that it might be. Well that’s it for the amoeba sisters and
we remind you to stay curious!