MUTABLE ALLELE CONTROLLED BY Dtl

HE gene A , in maize was first reported, with its mutant allele a,, by EMERSON (1918, 1921). In these reports and later publications by EMERSON and ANDERSON (1932) and LAUGHNAN (1948) the A , allele found in North American races was shown to be necessary for the production of anthocyanin pigments in various tissues of the corn plant. With the complementary genes A,, B, Pl, and R' or r', A , produces a deep purple pigmentation of the sheath, brace roots, auricle, leaf margin, husks, tassel, and anthers; with A,, Pry C , and R, it produces a purple pigment in the aleurone. With P it produces a bright red pigment in the pericarp. When a, is homozygous in the above genotypes, it causes the substitution of a brown pigment for purple in all tissues where anthocyanin normally appears, except for the aleurone, where there is no pigment. Various allelic combinations of the above genes can alter the type of pigment produced and the regions in which pigment is expressed, giving sun red, brown and green plants depending upon the genotype involved. The A locus is in linkage group 3 between lg, and et with 33 crossover units separating lg, and A, and 12 units separating A and et. It has been placed cytologically in the distal one fifth of the long arm of chromosome 3 (MCCLINTOCK 1931 ) . The mutant a which behaves as a normal stable recessive was shown by RHOADES (1938, 1941) to be mutable in the presence of the dominant factor Dt. This factor, located near the end of the short arm of chromosome 9, causes a to mutate to A in all the tissues where A vs. a differences can be seen. In the proper genetic background, the mutant areas appear as small dots of A tissue on a colorless aleurone, and as long narrow purple sectors on the brown sheath, culm, husks, etc. These sectors may extend into the tassel to give purple anthers which, depending on whether or not the sector includes the germ line, may transmit a mutant A allele in 50 percent of the pollen. There are known, at the present time, many A , alleles in addition to those reported by EMERSON in his original study. Most of these have arisen as mutants from the four original parent alleles A , a, Ab and ap and have been organized into several groups according to their phenotype, parentage, and mode of origin (RHOilDES 1941 ; LAUGHNAN 1949; NUFFER 1952). The compound nature of certain alleles of South American origin has been demonstrated by LAUGHNAN (1949). These alleles characterized as Ab have at