Abstract
Four isoflavone mutations of considerable biological and practical potential are described. Genetic evidence accumulated to date suggests the mutations to be simple recessives. A single gene can control the release of bound isoflavones. Single genes apparently also control the methylation of daidzein and genistein to formononetin and biochanin A respectively, and the development of isoflavones in normal quantities. Crosses between lines carrying the individual mutations lead to modified dihybrid Mendelian ratios.