It may be pointed out in passing that if, as Arkell assumes, the hornless races are due to the presence in them of an inhibitor for horns, the results can be worked out without postulating that the inhibitor is sex-linked. For example, if the hornless male and female be HHII and the horned male and female HHii, the F₁ horned males and hornless females will be HHIi. The germ-cells will be HI and Hi in each sex, which, by chance meeting, as shown below, gives the results obtained by Wood. Thus:
| HI | × | Hi.....female. |
| HI | Hi.....male. | |
| 1HIHI+2, HIHi+1, HiHi. | ||
These formulæ give 3 horned males, 1 hornless male, 1 horned female, 3 hornless females. This formulation, while appealing apparently to a different set of factors from those used by Arkell, is in reality the same in principle, since the heterozygous condition is here represented by Ii (instead of Hh) and sex determines that the heterozygous male is horned and the female hornless.
The genetic relations of the Merino with horned males and hornless females to the Dorsets, in which both sexes are horned (but in the male the horns are larger), must be different from the genetic relation in the other cross. There are two theoretical possibilities, viz., that a different factor for horns is present that is either an allelomorph or another different factor; or second, that a modifier is present in the Merino that keeps down the development of the horns in the female. An answer could be obtained by breeding Merinos to horned and to hornless and getting F₂ from both crosses. Arkell’s data is not sufficient to settle the question, because his numbers are often too small, but chiefly because it appears that there were two genetic types present in his flock of Merinos, one of which is characterized by scurs (very short horns) in the females, the other by hornlessness in the female. He found in a cross between a hornless father and Merino mother (that had knobs or scab-like growths) that the daughters had horns or scurs and carried a determiner for horns (as subsequent generations showed). On the other hand, in other cases where the Merino mother was without horns, her F₁ daughters had no horns. In both cases the F₁ sons had horns. Arkell cites this cross as “proving” that the knobs of Merino ewes depend for their development upon two horn determiners (H´H´). It is not at all evident that the results lead to such a conclusion, as other explanations will cover the case as well.
Arkell’s mating between Dorsets and Merinos (tables IX and XVI) corroborates his view “that the knob of the Merino female is represented in the germ-plasm by the double determiner.” The 5 F₁ sons had long horns, 3 F₁ daughters had horns present, and 2 had them absent (table XVI). If some of the Merino mothers used were homozygous for a factor that inhibits the development of horns in the female we can account for the hornless daughters, and if other mothers did not have this factor (or were heterozygous for it) we can account for the horned daughters. Evidently more evidence is needed. Arkell himself assigns a corresponding difference to the mothers in these cases, based on the observed fact that the mother that had knobs or scurs were the ones that gave birth to the horned daughters. If the above suggestion proves true, it shows that the Merino condition dominates the Dorset condition. The result is in harmony with the view that both have a common factor for horns, but that in addition the Merinos have a non-sex-linked modifier that holds down the development of the horns in the ewe.
What bearing have these results on the theory of sexual selection? Clearly the Merino male, as constituted at present, develops horns because he is a male, but only in the sense that his testes secrete some substance that makes his horns grow. That maleness does not in itself necessarily produce horn is shown by the absence of horns in the Suffolk breed. Is it the same factor, present in the Merino, that produces horns in both sexes of Dorsets when homozygous and in the male only when heterozygous? If originally the ancestral race had no horns, the appearance of factors for horns would, even in a heterozygous condition, have sufficed in the males for the development of horns. If this gave them any advantage either over the enemies of the race or in the eyes of the female, such factors might be perpetuated, and through transferrence to the females ultimately become homozygous in both sexes. Both would then have horns, whether horns were or were not of any advantage to the female, which would have them because they have an advantage to the other sex.
Because the genetic evidence shows that a single factor difference between the breeds with and without horns accounts for the horned condition in one of them, it by no means follows that horns as they exist arose as a single mutant factor change. True, they may have arisen as a new single factor difference, but the Mendelian evidence can not be claimed as evidence for this view. The a priori argument based on the relation of horns in an adaptive sense to the rest of the body would appear rather to indicate that they could not have arisen at a single mutational step.
Concerning the still broader bearing of this evidence on the theory of sexual selection, two distinct questions are involved: first, how has the present racial difference in horns arisen in domesticated sheep, and secondly, what was the original condition of sheep. Reversing the order of these questions, we find that sheep were domesticated in Asia and Europe before the dawn of history. “Whether our well-known and useful animal is derived from any one of the existing wild species, or from the crossing of several, or from some now extinct species, is quite a matter of conjecture” (Flower and Lydekker’s “Mammals”). Most of the wild species of the genus (of which about 12 are recognized) have horns in both sexes, but larger in the male. There are 3 wild species in which the horns are lacking in the female, according to Flower and Lydekker. If these have been crossed into the domesticated breeds the condition shown by the Merino may go back to the wild state. The third condition found in domesticated races, viz, hornlessness, may have appeared under domestication. Such a change might have arisen in either of the two other types and would be comparable to well-known losses of characters shown by domesticated animals and plants. These losses of characters are usually ascribed to actual losses of genes; any lost gene in the complex of factors necessary for the production of horns might cause such a change. But there is no advantage, in fact, in ascribing the loss in the character to a loss in one of the factors producing that character, for any change of any kind in the factor complex might bring about the same result and the evidence from multiple allelomorphs should put us on our guard against the all too easy assumption that a loss in a character involves necessarily loss of a factor in the real sense in which loss is used in ordinary speech.
The operative and genetic evidence for sheep shows that if the horns in the male were developed through natural or sexual selection we should expect them to develop also in the female. The greater development in the male seems to be due to secretions from the testes which probably are due to special factors that call them forth, but whether such factors were also acquired to reinforce the effects being produced through selection or were already present (reinforcement for horns being only a by-product of their activity) can not of course be known. We can suppose that special factors that suppress the development of horns in the female may have arisen in the wild or in the domesticated races and have been perpetuated because of some imagined benefit conferred; or that in certain races factors were already present that kept down the development of horns in the female. In any case such factors do not cause their effects through secretions from the ovary, because after ovariotomy horns do not develop; nor are they sex-linked factors. Any speculation as to how natural or sexual selection has brought about the evolution of the horns in sheep must reckon with the conditions imposed on such speculation by the preceding information. So far as I can see, it leaves the situation in this respect neither better nor worse off than before.
In deer the effects of castration are well known, but there is no genetic evidence to show the kind of factors involved, since no crosses have been made between species with differences in their horns. If the young male deer is castrated before the antlers have appeared, no horns develop. If castrated at the time when the antlers have begun to develop, incomplete or imperfect development follows. The antlers remain covered with the velvet, and are said not to be thrown off periodically as in the normal male. If the adult stag with antlers is castrated, the horns are precociously dropped, and, if replaced at all, the new antlers are imperfect and are not renewed. I do not know of any cases in which females have been spayed, but no doubt the ovaries must sometimes become diseased. There are, however, a few records of horns developing in this sex in old age, or presumably after disease of the ovaries. Both male and female reindeer are horned. Castration produces no effect on the development of the horns.