“…This natural mutant collection includes varieties that either lack or underproduce Kunitz trypsin inhibitor , seed lectin (Pull et al, 1978), p-amylase (Hildebrand and Hymowitz, 1980), lipoxygenase (Hildebrand and Hymowitz, 1981), glycinin (Scallon, Dickinson, and Nielsen, 1987;Cho et al, 1989), p-conglycinin (Kitamura and Kaizuma, 1981), and urease (Kloth, Polacco, and Hymowitz, 1987). In each inbred lhe, the defect is the result of a mutation that is inherited as a simple Mendelian recessive (e.g., Orf and Hymowitz, 1979). Severa1 seed protein gene mutations have been studied and their molecular lesions have been characterized .…”