In the previous note, Woodman used one of our new Adh1 mutants to better understand the organ-specific "reciprocal effect." Over the last three years, we have used chemical selection procedures to recover Adh1-deficient mutants via resistant pollen grains shed from mutagenized plants. Accelerated heavy neon (400 MeV/amu Ne10+) has been most useful. Our first 69 radiation-induced mutants have undergone preliminary characterization, and our methods have been detailed (M. Freeling and D. S. K. Cheng, 1978, Genet. Res., in press). Adh1-S1951a is one of the mutants generated by this approach; the "a" denotes a derivative of the original aberrant. This mutant is stable and linked closely with an electrophoretic site in the Adh1-S structural gene. Its phenotype includes underproduction of ADH1-S subunits in the scutellum, and--reciprocally--overproduction of ADH1-S subunits in the anaerobic primary root. The mutant has no trans effects. The original F1 seed, of the genotype Adh1-F/Adh1-S1951 (see Woodman's figure), was recognized as an underproducer in the scutellum, but this characteristic was not stable upon backcrossing to the Adh1-F parent. Electrophoretic analyses of scutellar slivers from backcrossed progeny (BC1) found that most Adh1-S alleles appeared to be wild-type, one (of 75 transmissions) showed underproduction, several displayed overproduction, and some hyperploids for Adh1 were transmitted through the F1 male gametophytes and were detected in a test-cross. We call these backcrossed individuals "derivatives." I have looked at meiotic chromosomes in some of these Adh1-F/Adh1-S1951 derivatives. Extra centric fragments are usually present, and chromosome one appears to be involved in a complex rearrangement which leads to some bridges at both anaphases. I did not analyze the single Adh1-1951a derivative (underproducer) and much further chromosomal work will be necessary if we decide it is worth it to sort out these complex aberrations. The original F1 gave 7% abortion. The underproducer derivative, Adh1-S1951a, was backcrossed to the Adh1-F parent once again (BC2). Now the Adh1-S1951a mutant behaved as a stable allele of Adh1 with a phenotype as described.
The "reciprocal effect" regulatory behavior of Adh1-S1951 would not be expected of a structural gene mutant. All of the about 50 Adh1 mutants characterized by Schwartz, including those which I have tested for intragenic recombinational success, can be explained as lesions confined to the structural gene. The product of Adh1-S1951a appears nonmutant in electrophoretic mobility and thermostability; a comparison at the peptide level is in progress. Chances seem high that heavy-ions induced a complex aberration which, in turn, generated a stable mutant/aberrant in the cis-acting, programmable component of Adh1.
The origin of Adh1-S1951a parallels that of maize transposable element systems in several obvious ways (e.g. B. McClintock, PNAS 36:344, 1950 for the origin of Ac-Ds).
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