The interpretation of autosexing

1. Autosexing breeds of fowl may be divided into those which carry the sex-linked gene for barring (B), and those which do not. In the former group, the autosexing properties are due to the imperfect dominance of B. 2. A table (Table 2) is presented showing the possible dominance relations between a sex-linked gene which is a hypomorph, hypermorph, antimorph, amorph or neomorph, and its wild-type allele, both without dosage compensation, and in conditions of partial and full dosage compensation. 3. A study of the ‘ticks’occurring on birds having various constitutions for the two sex-linked loci B and S silver) shows that the ticks are due to somatic elimination of part of an X-chromosome. It shows further that B is a neomorph (b having no action on pigmentation) without dosage compensation, or possibly a hypomorph (b having a very weak action in the same direction as B) with, at most, a slight degree of dosage compensation. This in itself is sufficient to explain the autosexing properties of barred breeds, without resorting to the improbable assumption that females have a Y-chromosome which carries b. 4. Anomalies are pointed out in the dominance relations at several sex-linked loci (w, A, B, Hw) ofDrosophila melanogaster, which are difficult to explain on Muller’s theory of dosage compensation. 5. There is no reason to attribute any autosexing effect to either allele at the silver locus of the fowl. There is some evidence to suggest that the sex hormones, rather than a specific sex-linked gene with a dosage effect similar to that of B, are responsible for autosexing in non-barred breeds. On whether the testicular or the ovarian hormone is responsible, the available evidence is conflicting.