ABSTRACT
The ragged mutation arose in a crossbred stock of mice in which a translocation had been induced by X-irradiation five generations earlier. In the heterozygous opossum embryos, auchene and zigzag follicles are present at birth, but they do not complete differentiation. The retarded follicles in homozygous and heterozygous mice did not produce hairs and lacked sebaceous glands. Follicular density for Ra/+ mice was normal prior to birth but approached normal after birth. Follicle formation is delayed more in homozygous ragged and opossum mouse embryos. The hair cycle in both mutants is asynchronous throughout the life of the mutant mouse. Subsequent studies revealed that incidence was not controlled by a Chy gene linked with ragged; rather, it is modified by one or more genes unlinked to Ra and two mutant genes (fi and reader) linked to Ra and another on Chromosome 1 (py).
