In the previous lesson we learned that inhibitor genes can confuse our
understanding of the dominant or recessive nature of traits that we
may be interested in. Inhibitor genes, besides acting as single
genes, can also be duplicate genes or dominant complimentary genes
acting on either a single gene, duplicate gene or dominant
complimentary gene. I'll cover complimentary dominant inhibitor genes
in some detail because it is likely that you will find these types of
inhibitor genes involved in flower color inheritance. For this and
future discussions I am going to use the term "effect gene" as a
general term for any gene that mediates the conversion of a precursor
to a end product in contrast to an inhibitor gene which blocks the
conversion of a precursor to an end product.
Dominant complimentary inhibitor genes acting on either a single effect gene or a dominant complimentary gene system can produce some interesting side effects. I'll discuss this first with a dominant complimentary gene acting on a single effect gene.
Lets go back to our red-white flower example where red flowers are a dominant trait controlled by gene R. We can take two true breeding red flowers, cross them and get all white F1's. We can explain this as RRJJkk x RRjjKK where R produces red flowers and J and K are dominant complementary inhibitor genes that prevent gene R from converting a colorless precursor to a red pigment. In our example both parents are red because they are homozygous dominant for the R gene and both parents lack one of the dominant complimentary inhibitor genes. The F1 is now RRJjKk which is white because the F1's have the complimentary inhibitor gene in an active state.
To figure out the segregation in the F2 generation we need to figure out the frequency for the effect trait, in this case red flowers, and multiply that by the frequency of the inhibitor genotypes that do not inhibit the effect gene. In this example the inhibitor genotypes J_kk, jjK_ and jjkk will not inhibit the R gene. These have frequencies (3/4 x 1/4) + (1/4 x 3/4) + (1/4 x 1/4) which sums up to 7/16 for the frequency of genotypes that will not inhibit the red gene. In this example the red gene is not segregating, so the frequency for the RR genotype is 1. This, the frequency of red genotype times the frequency of inhibitor genes not inhibiting the effect gene is 1 x 7/16, so in the F2 generation we will see a 7:9 segregation ratio for red:white flowers. We took two true breeding red flowers, got all white F1's and in the F2 generation have more white flowers than the dominant red flowers.
We can also get the same exact results in the F1 and F2 generation from crossing a true breeding red flower with a true breeding white flower. If we take the cross RRjjkk x RRJJKK, red x white, we get the same white flowered RRJjKk genotype in the F1 generation as for the previous example and the F2 generation will give us a 7:9 ratio for red:white. In this case we would think that white is dominant, but in our previous example we might be wondering where the white trait came from and why it is more prevalent in the F2 generation than our dominant red flowers. Examples like this can eventually be figured out by making backcrosses, test crosses and other crosses to known genotypes, but a lot of confusion can exist while all of this is being worked out.
Dominant inhibitor genes acting on dominant complementary effect genes can add even more confusion and the segregation ratios can get to be difficult to figure out. No matter how complicated the cross, to figure out the segregation ratios all you have to do figure out the segregation frequency that gives the effect (in our case red flowers) and multiply it by the frequency of the genotypes that do not produce an active inhibitor. The number of different possible crosses that we could consider becomes rather large because we have four genes that are segregating. I'll just give a few interesting cases. We will use our red-white flower example, but now red flowers are caused by the dominant complementary genes A and B, and the dominant complimentary inhibitors genes are J and K.
Here is an interesting case that may confuse people. Lets make the cross AAbbJJkk x aaBBjjKK, white x white. The F1's will be AaBbJjKk, which will be white. However, in the F2 generation we will get some plants with genotypes A_B_ which will produce red flowers if the inhibitor genes are inactive. In this case the frequency of the A_B_ genotype is 9/16, but only 7/16 of those plants will also be of genotype J_kk, jjK_ or jjkk, so the frequency of red flowers in the F2 generation is 9/16 x 7/16 or 63/256 which will be a 63:193 ratio for red:white. This ratio will most likely appear to us as a 1:3 ratio. We crossed two white flowers, got all white F1's, but now in the F2 generation we are getting about one quarter red flowers.
We can also get the same F1 genotype and the same segregation in the F2 generation from a red x white cross of genotype AABBJJkk x aabbjjKK or AABBjjkk x aabbJJKK. In this case the F1's are white and the 193:63 segregation ratio for white:red would look like a 3:1 ratio and we may conclude that white was a single dominant gene! Again, backcrosses and other crosses would eventually provide us with the correct inheritance, but it could take considerable effort.
By now, many readers may be bored with all the niceties of the mathematical calculations and the complexity that has been added. Unfortunately, many of the daylily traits we may be interested in may follow these complex inheritance patterns presented here. For the practical daylily hybridizer the exact segregation ratios may not be all that important. However, a basic understanding of how inhibitor and effect genes can interact can help explain some of those strange results that show up, especially with flower pigments.
If you cross two plants and get unexpected traits in the F1 generation first suspect that dominant complimentary genes are involved. For example, if you cross two plants that both lack anthocyanidins, (red or purple) and get red or some variation of purple, it is likely to assume that this is a dominant complimentary gene system at work. In many plants the presence or absence of anthocyanidin pigments is controlled by dominant complimentary genes.
If you are getting conflicting results where a trait sometimes appears to act as a recessive trait and other times as a dominant trait suspect inhibitor genes to be involved. Also suspect inhibitor genes if you loose a trait that otherwise appears to act as a dominant trait.
All of us who have been following the progress of daylily hybridizing lately are well aware of how quickly the gold edged and picotee edges have emerged and become prominent in the market. Inheritance at the tetraploid level is greatly complicated compared to diploids, but I would not be surprised if these edges involved inhibitor genes. A general discussion of some of the issues involved with tetraploid inheritance will be covered at a later time.