During the past few years, a number of terminal deficiencies of the short arm of chromosome 9 have been isolated. Each deficiency arose as the consequence of a meiotic breakage of the short arm of chromosome 9 following crossing over in plants homozygous for a chromosome 9 with a duplication of the short arm or for a structural rearrangement of the segments of chromosome 9. In each case, the extent of the deficiency was determined at pachytene in the F1 plants which had received a normal chromosome 9 from one parent and a recently broken (deficient) chromosome from the other parent. Tests showed that deficiencies which ranged from minute to one-third of the distal segment of the short arm were all female transmissible. Those which extended into the first distinct chromomere were transmissible through the pollen. None of the longer terminal deficiencies were male transmissible. Because of the male and female transmission of the very short terminal deficiencies, plants which were heterozygous for these deficiencies were self-pollinated to determine if viable endosperms and embryos could be obtained which were homozygous for these deficiencies. In these F1 plants, the normal chromosome carried c and the deficient chromosome carried C. The C mutant is located in the short arm within the 5th or 6th chromomere from the distal end. In these F1 plants, 30 individuals were classified as having received a broken chromosome 9 which was deficient for only the knob. Self-pollinations of these heterozygous deficient plants gave typical ratios of 3 C to 1 c. The endosperms and embryos in both classes of kernels were normal. Plants arising from both the C and c kernels were likewise normal in appearance. Cytological examination of some of these F2 plants showed the presence of the two deficient chromosomes 9. It may be concluded that a homozygous deficiency of the knob does not obviously alter the appearance and functioning of any tissues.
Seven of the original F1 plants were classified as having a chromosome 9 which was deficient for the knob and the adjacent segment of thin chromatin which joins the knob with the first distinct chromomere. Self-pollinations of these plants likewise gave typical ratios of 3 C to 1 c. The endosperms and embryos were normal in appearance. In all 7 cases, the seedlings arising from these kernels segregated in the ratio of 3 green to 1 pale-yellow. The pale-yellow seedlings are normal in morphology but die following exhaustion of food supplies in the kernels. Linkage of the pale-yellow phenotype with C, carried by the deficient chromosome, was obvious in each case. Through genetic and cytological means, it was possible to determine in each case that the recessive pale-yellow phenotype is produced as a consequence of the homozygous deficiency. Intercrosses between plants heterozygous for these 7 pale-yellow mutants showed that all 7 were either identical or allelic. The recessive mutant yg2 is known to be located close to the end of the short arm of chromosome 9. Combinations of a chromosome 9 carrying yg2 with any of the 7 deficient chromosomes 9 produced only normal green seedlings and plants. It may be concluded that the deficiencies which produce the pale-yellow phenotype are not long enough to include the Yg2 locus.
In six F1 plants, the broken chromosome 9 was classified as being deficient for a terminal segment which extended into and included a part of the first distinct chromomere. These deficiencies were slightly longer than those which produced the pale-yellow phenotype. Following self-pollinations of these plants, normal F2 ratios of 3 C to 1 c appeared in four of the six cases and a slight reduction of the C class in two of these cases. When these kernels were germinated, white seedlings segregated in ratios expected from a recessive mutant. In all cases, linkage of the white seedling mutants with C was obvious. It was possible to determine for each case that the white seedling phenotype resulted when these seedlings were homozygous for the deficient chromosomes 9. Intercrosses of heterozygous deficient plants of all 6 cultures were made to determine the allelic relations of the white seedling mutants. White seedlings segregated in the F1 following all 15 combinations, indicating that the white seedling mutants were allelic if not identical. Intercrosses between plants heterozygous for the 7 pale-yellow producing deficiencies and the 6 white producing deficiencies gave rise to the typical pale-yellow phenotype in one-fourth of the progeny of all 42 crosses. It was determined that the pale-yellow phenotype arose following combinations of the two deficient chromosomes in a zygote. Thus, the deficiency mutants pale-yellow and white are allelic. Pale-yellow is dominant over white. This would be expected because the residual homozygous deficiency following combinations of the two deficient chromosomes is only that which would produce the pale-yellow phenotype.
Plants heterozygous for the 6 white seedling producing deficiencies were crossed by plants homozygous for yg2. In the progeny of all 6 crosses, a ratio of 1 green plant to 1 yellow-green plant appeared. Appropriate tests showed that the yellow-green plants were those which had received the deficient chromosome 9 from the heterozygous parent. Therefore, it may be concluded that the white mutants are allelic to yg2, with yg2 dominant over white. This would be expected if the nominal deficiencies causing the white seedling mutants included the locus of Yg2. From the point-of-view of genetic analysis, the pale-yellow and white seedling mutants are comparable in all ways to other known recessive mutants in maize. The allelic expressions of pale-yellow and white and yg2 and white, and the non-allelic expression of pale-yellow and yg2 would be difficult to interpret following a purely genetic analysis. These results are readily interpretable when the cytological conditions are known. The phenotypic expression following combinations of any two of the three mutants may be considered a reflection of the residual effects of over-lapping deficiencies.
The mutants pale-yellow and white are repeatedly produced following the meiotic breakage of chromosome 9. Among 2577 such recently broken chromosomes 9 which were tested, 55 gave rise to the pale-yellow phenotype and 33 to the white phenotype. In contrast to most mutation inducing agents, the chromosomal breakage mechanism is a "mutation" inducing process which "induces" the same mutant time and again.