Even if these figures are still not statistically sufficient from my point of view, there is a clear difference of around 7% between colored offspring from solid Appaloosa mares and solid outcross mares. Thus there is clear evidence that monochrome Appaloosas have fewer colored foals in their offspring than monochrome outcross matings.

If this now corresponds to a significantly less whitening color in the colored foals, then one can at least in theory assume the existence of a braking agent. That would mean that the braking action would have an influence on the spread of the whiteness.

What would the purpose of this gene be?

When we look beyond the Appaloosas, we cannot turn a blind eye to an aspect of whitening.

1. The lethal white in the paints, too much white coloring is coupled with an intestinal obstruction and thus the death of the foal.

A white coloring in Appaloosas does not have these consequences. That could be a result of braking.
Another indication of the existence of such a gene would be the number of pure-bred (homozygous) foals from the mating of colored Appaloosa x colored Appaloosa. From a purely statistical point of view, this should be 25%.

As can be seen from an earlier study by the University of Verginia, here 70 matings of few spot x other Appaloosa skin markings were examined, the number of few spot foals resulting from this was not 50%, as would have been expected, but only 10%. Since this classification was only made by phenotype, the real classification that can be carried out today by genetic analysis could well result in a significantly higher number of homozygotes. But they didn't look like homozygotes about the existence of such inhibiting genetics

or even confirmed suppressive genetics.

This, too, is further evidence of the existence of such a braking device.

If the mating of a colored stallion with solid Appaloosa mares results in differences in color inheritance both in terms of the extent of the white factor and in general in the transmission of the Lp gene to matings with solid outcross mares, then this can logically only mean that this stunted horse has a close connection with must have the lp gene. Despite this close connection, it must be a separate inheritance that is probably only homozygous.

If solid Appaloosa mares carry this stunt then this is evidence that it is independently inherited. Definitive evidence could only be obtained by a comprehensive study that takes the following aspects into account:

Mating of one or more few spot stallions with solid Appaloosa mares and solid outcross mares to prove that the whiteness of solid Appaloosa mares is reduced.

Mating of one or more heterogeneous stallions with solid Appaloosa mares and solid outcross mares in order to determine a general difference in the lp gene transmission. To be on the safe side, the heterogeneous colored stallions would have to come from outcross matings.

If you add 65 foals from the statistics of the ApHCG, which are presumably from homozygous stallions, the percentage of colored foals changes from 76.77% to 67.44%. Disregarding the fact that there are also homozygous mares, the number of colored foals (heterozygous x heterozygous) would have to be 75% and, including homozygous mares, around 83.5%. These facts also speak in favor of the existence of such a braking system.

Implications for breeding?

First question: Is there a disease-related disposition in Appaloosas that can be associated with the Lp gene and is this disposition proportional to the white drawing? In this case, the brakes would have a positive effect on hereditary health and would therefore be worth preserving.

If this were not the case, one would have to think of ways to minimize it.