In maize, there is a non-random distribution of known mutants in the genome. Chromosome 8, for example, has only six known genes whereas the least number known on any other chromosome is 20. Furthermore, all known mutants in chromosome 8 are in the distal quarter of the long arm. Rhoades (Amer. Naturalist 85:105-110, 1951) suggested that the non-random distribution of known mutants in maize might be an indication of redundant chromatin in segments where relatively few genes are known.
I have begun a long-term study using monosomics to determine if there really are fewer genetic loci capable of being mutated on chromosome 8 than on other chromosomes. The procedure is outlined below.
R/r-X1 plants are crossed as female parents by pollen parents carrying a single recessive seedling mutation. The pollen of the male parent is treated with a mutagen such as ethylmethansulfonate (EMS) using standard procedures. All progeny expressing the seedling mutation are monosomic for the chromosome bearing the marker mutant. One simply grows plants expressing the mutant phenotype and examines these plants for the presence of a second mutant phenotype. The second mutant phenotype could be attributable to a dominant mutation induced anywhere in the genome (these are rare in maize) or a recessive mutation on the monosomic chromosome. Any mutation affecting the sporophyte morphology would be detected in this way. It is also possible that the mutagen would induce a new mutation which has a phenotype similar to the one used to identify the monosomic. If the F1 plant was monosomic for the chromosome carrying this new mutation, it can be readily determined by testcrossing to plants recessive for the mutant in the original male parent.
Each plant expressing the marker mutant will also be selfed to determine if any mutation affecting kernel morphology was induced by the mutagen. If all kernels produced by the monosomic were mutant for a new phenotype, it would indicate that a mutation was induced on the monosomic chromosome that affects kernel morphology. Furthermore, these progeny would be homozygous recessive both for the marker mutant gene locus and the newly induced mutant gene locus.
Each monosomic carrying a new mutation will also be crossed by a standard inbred line. All F1 progeny will be heterozygous both for the marker mutation used to identify the monosomic and the new mutation, and the genes would be in coupling: These F1 progeny could then be crossed by plants produced by the selfed monosomic (which are homozygous both for the marker mutant and the newly induced mutant). This will greatly simplify mapping of the new mutants.
I am mutagenizing pollen from plants carrying recessive marker mutations on chromosomes 7, 8, or 10. 1 will determine the frequency of mutations on chromosomes 7, 8, and 10. 1 will determine if the frequency of mutants induced on chromosome 8 is similar to the frequency of mutation induction on the other chromosomes tested. Also, I will determine if most of chromosome 8 is actually refractory to mutation induction or if the lack of known mutants on chromosome 8 is a fortuitous mapping artifact. It is hoped that through this program it will finally be possible to map chromosome 8 in maize. Supported by ERDA Contract No. EY-76-S-0L-2121.
David F. Weber
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