My illustration may give, however, an entirely erroneous idea as to the chance of a recessive character contaminating the race. If one can control the matings, so that out-breeding takes place each time, the result would undoubtedly be like that in our diagram; but what chance is there for a recessive character, that is neither beneficial nor injurious, if left to itself, to contaminate widely the race with its gene? The answer is that for any one defect there is hardly any chance at all. On the other hand, there is always a possibility that a defect may become widespread despite the chances against each in turn. If a recessive character is selected against each time it appears on the surface, the chance is extraordinarily small that the gene for such a character could ever become widespread in a race. If the recessive character is advantageous, its chance is somewhat better, but still the chance that it may be lost is very great.
Let us turn for a moment to the inheritance of a Mendelian dominant character, and to simplify the situation let us first assume that the character itself is neither advantageous nor disadvantageous.
It is popularly supposed that if a trait is dominant it will be expected to spread more widely in the race than will a recessive character. This is owing largely to a verbal confusion. Colloquially we think of dominance as meaning spreading. A dominant nation, for example, is one that is spread widely over the face of the earth. But a Mendelian dominant should carry no such implications. A dominant gene, if crossed into a race, will stand the same chances of being lost as a recessive gene, [Fig. 3].
The situation is similar in many ways to the inheritance of surnames in any human population. A new surname introduced is likely to disappear after a few generations. There is a bare chance, however, that it may spread.
Fig. 3. Mating of short-fingered and normal individual (the short-fingered character is dominant), giving in F₁ normal and short-fingered individuals in equal numbers. If the latter is out-bred to normal again, half the next generation is normal and half short-fingered.
Of course if a dominant character is advantageous in itself, it will have a better chance of spreading through the race, than will an advantageous recessive character, because every hybrid that carries one dominant gene shows also the character, which increases the chance that it will propagate and spread the genes. But, on the other hand, if a dominant character is injurious it will have a smaller chance of spreading than will an injurious recessive character; for, the recessive may be carried by the hybrid without showing itself, and therefore will not place the hybrid individual at a disadvantage.
An excellent illustration of dominance is that recently published by Mohr. He has traced, through five generations of a Norwegian family, the inheritance of a shortened first digit. In the history of this case there is one record that is extraordinarily interesting. A child was born that was so completely crippled that it died in infancy. One parent was short fingered; the other, a cousin, was probably also short fingered. It is possible that the child had a double inheritance of this character; it was a pure dominant. If this is true, then it appears that this character can survive to maturity only in the hybrid condition. As a matter of fact, in other animals there are some well-recognized cases of this sort. That of the yellow mouse is the best known. Yellow is a dominant and in double dose it kills; therefore when yellow is bred to yellow all the pure yellows die. The hybrid yellows and the pure blacks (in [Fig. 4]) survive. Here yellow is discriminated against in the embryo; but, being dominant, it still appears twice as frequently in each generation as does the alternate character (here black). In the fly, Drosophila, we have at least 25 dominant lethal characters, but as yet we have no knowledge as to why such a high percentage of dominant characters should be lethal when homozygous.