--Bill Cook and Don Miles

A Mutator mutagenesis experiment was conducted with the purpose of isolating Mu-induced high chlorophyll fluorescent (hcf) photosynthesis mutants. Twenty colorless kernels obtained from D. Robertson (DR 78-79-8091/7092-8) were grown as male mutagenic parents and crossed to 1087 ears of Mo17 or W23. Thirteen hcf mutants were isolated and characterized photochemically and biochemically. Several other mutations with phenotypes detectable at the seedling stage were isolated as well.

Ten of the hcf mutant stocks as well as one blue fluorescent and one glossy mutant were crossed to 19 B-A translocation stocks (obtained from M. G. Neuffer) in order to determine their chromosome arm locations. Seven of the mutant loci were mapped in this way. Two of the mapped loci (hcf103 and gl*-1258) were allelic to other mutations which were isolated independently in the current experiment (hcf114 and gl*-1253-6). The chromosome locations of two other loci, hcf3-Mu and bf2-Mu, were deduced on the basis of their allelism to previously mapped loci, hcf3 and bf2.

Among the 11 mutant loci which were mapped to chromosome arms, 7 were located on 7L (uncovered by 7Lb). 31 EMS-induced hcf loci were previously mapped using B-A translocation stocks (Miles et al., in: Molecular Biology of the Photosynthetic Apparatus, Cold Spring Harbor, 1985).

Table 1. Chromosome arm locations of Mutator-derived mutations.

Seven of the 31 EMS-induced loci are located on 1L and four are on 6L. The remaining 20 EMS-induced loci are scattered among all of the other maize chromosome arms except those of chromosome 8 (one of the mutations in the current experiment has been mapped to 8L; Cook et al., MNL 61:44, 1987). It has been assumed, based on these data, that hcf loci are not clustered predominantly on one or several chromosome arms but are scattered randomly about the genome. Therefore, we tentatively interpret the high percentage of loci located on 7L in the present experiment to result from characteristics of the mutagen rather than clustering of loci on 7L.

There is evidence that both Ac and Spm transpose to physically linked chromosomal locations at a higher frequency than they transpose to unlinked positions (Peterson, Theor. Appl. Genet. 40:367, 1970; Greenblatt et al., Genet 108:471, 1984). To our knowledge, no published information demonstrating similar behavior by Mu elements is available. However, one explanation of the unexpected clustering of loci on 7L in this experiment is that a single Mu element, located on 7L, is responsible for all or most of the mutations located on 7L. The remaining loci mapped in this experiment (located on 1S, 5S, 8L, 9S and 10L) may have been tagged by the same element or by other, less active, elements which are located on those arms.

While we believe that these results may shed light on an interesting aspect of Mu transposition, we draw no firm conclusions from them. The mutagenesis and screening which yielded these new mutants were not designed to evaluate Mu transposition. Furthermore, the size of the experiment was not sufficient to either support or refute any particular hypothesis. Our limited knowledge of the mechanism(s) of Mu transposition combined with our expanding appreciation of the complexity of the Mutator transposon system(s?) (Talbert et al., MNL 62:59, 1988) continues to limit the usefulness of Mutator as a transposon tagging system. It is our hope that these results might be useful to those involved in the analysis of Mutator activity.

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