EPD-OLOGY

ADDITIVE AND NON-ADDITIVE GENETIC EFFECTS

by Darrell Wilkes, Ph.D., International Brangus Breeders Association (IBBA) executive vice president

In the last EPD-ology column, we discussed the most important equation in animal genetics. Namely, P = G + E, where P equals the phenotype such as yearling weight; G = the genetic influence on yearling weight, and E equals the environmental effect on yearling weight (think nutrition). We illustrated how vastly different environmental conditions can make two animals appear much different than they really are from a true genetic viewpoint. The computation of EPDs is designed to sort out the genetic effects from the environmental effects. In this column, we attempt to expand understanding of the genetic effects.

Genetic effects are broadly divided into two categories: Additive genetic effects, and Non-Additive genetic effects. Any attempt to explain the difference in a single column (as opposed to a stack of books on genetics and statistics) is going to over-simplify the subject, but that cannot be avoided.

Let’s assume that a trait like yearling weight is affected by only 5 pairs of genes. It is more likely that dozens or hundreds of genes are involved, but we’ll assume that only 5 are at play. Further, we will assume that the large letter for each gene adds 5 lbs of yearling weight, and the small letter adds nothing. Hence, an animal that is homozygous for all the “large” alleles will have a 50-lb yearling weight advantage over an animal that is homozygous for all the “small” alleles. Over time, if a breeder selects aggressively for yearling weight, he or she could “lock in” the large alleles and create a population of animals with a rock-solid 50-lb advantage. AA + BB + CC + DD + EE = 10 + 10 + 10 + 10 + 10 = 50.

These gene effects are called “additive” for the simple reason that their individual effects simply add up to a final result. If there was no environmental variation to create confusion, a breeder could compare two animals and know exactly what their true genotype differences are. If animal Alpha was 15 lbs heavier than animal Beta, you would know precisely that animal Alpha had three more “large” alleles than animal Beta. Life as a cattle breeder would then be too easy, and maybe even boring. In the real world, environmental effects come into play which can actually result in an animal with a poorer genotype having a superior phenotype – i.e. an animal with only 5 “large” genes actually having a heavier yearling weight than an animal with 10 “large” genes. It happens every day in every herd, guaranteed. But even with the curve balls thrown in by random environmental effects, those animals with more of the “large” alleles will tend to outweigh those with more “small” alleles. So even though some selection decisions are genetically wrong, there will be a genetic trend over time that is consistent with the selection pressure that is placed on the population. To state the obvious: if you have good data and select for more weight, you’ll get more weight. Note the emphasis placed on the phrase “good data”. If you have poor data or no data, genetic change in the direction that you desire will probably not happen.

Environmental effects are not the only thing that can confuse the simple additive model of genetics. Non-additive genetic effects can confuse the picture also. This does not mean that non-additive effects are bad. They actually can be very good, but the point is that they can create confusion.

Unlike the simple additive model where an animal with the “AA” genotype is superior to the animal with either the “Aa” or the “aa” genotype, non-additive effects are a bit more difficult to deal with. Again, admitting to the oversimplification, let’s assume that the “A” allele and the “a” allele each code for slightly different proteins, both of which are advantageous. Hence, the most preferred genotype in this case would be the heterozygote “Aa”. This is where you must stop thinking of the “large” allele as being dominant or superior, and the “small” allele as being recessive or inferior. They are not additive as in the above example. Each has their role, and both are positive. This is what we call heterosis. It is synonymous with heterozygote. The problem is, you cannot select for heterosis.

Let’s assume that we have two parent animals, both of which were judged to be superior to their contemporaries and both of which were heterozygous -- “Aa”. They are selected to be parents with the goal of making the next generation better (i.e. following the additive genetic train of thought). This is where we get to use the Punnett Square that we all learned in high school biology. Let’s assume we flushed the cow and ended up with 4 full siblings. The Punnett Square below shows the expected genotypes of the four progeny:

Note that 2 of the four progeny are heterozygous and, therefore, equivalent to the parents. The other two are homozygotes and are inferior in performance to their heterozygous siblings and their parents. On average, the 4 progeny actually have lower genetic merit than the parents that mated to produce them. That is, two are equal to the parents and two are inferior. So, on average, the group is inferior. If you select the two superior animals, the heterozygotes, and mate them, you get the same result. The point is: you cannot select for heterosis.

Non-additive genetic effects such as heterosis are much like environmental effects in that we must try to sort them out because they are random and cannot be predicted. They do not carry forward to the next generation in a simple way like the additive genes do. In simple terms, EPDs represent additive genetic effects. We often talk about heritability. Heritability is relative to the additive genetic effects. When we say that a trait is 40% heritable, what that means is that 40% of the observed phenotypic variation is due to additive genetic effects. The other 60% of the variation is due to environment and non-additive genetic effects.

If you were taking a college course in quantitative genetics, you normally wouldn’t cover non-additive effects until at least half way through the semester. So, if you are following this topic with a clear understanding, you are well ahead of the game.

I’ll close this article with a “cake and icing” analogy so that you do not start thinking of non-additive genetics as your enemy. Composite breeds like Brangus have an advantage over “straightbred” cattle because of retained heterosis. Heterosis is a good thing, even though it makes genetic evaluation a bit more complicated. In genetic terms, the “cake” is the base of everything. The “cake” is the additive genetic merit of your herd. As you select for certain traits using EPDs you are creating a taller cake – that’s good. The icing is on top, and the icing is the retained heterosis. You cannot stack icing. It gets gooey and spreads out. The total height of your dessert is the cake plus the icing.

There is a natural tendency for breeders to look at the EPDs of an animal and then also look at the individual phenotypes such as birth weight, IMF percentage, etc. and make a judgement as to whether the EPDs are consistent with the phenotypes. Purely from a scientific standpoint, there is little value in this because the phenotypic data are already baked into the EPDs and every effort has been made to sort out the “noise” caused by environmental effects and nonadditive genetic effects. Breeders will always want to look at actual phenotypes. It is human nature. But don’t let the actual weights and measures overshadow the EPDs because the EPDs are the most informative values available.