Lindstrom (1924) reported that the w2 mutation not only produced recessive white seedlings, but also adversely affected endosperm development. The two genetic effects were tightly linked, suggesting pleiotropy or mutation of two adjacent loci. Discrimination between these two mechanisms would be possible if the two traits were separable by crossing over, but in Lindstrom's time the necessary flanking markers were not available. Even if they had been, the lethality of the white seedlings and the existence of modifying genes affecting endosperm development would have made it difficult to discriminate between the two alternatives. However, some recent observations throw some light on the nature of the w2 mutation.
Our DfK10(F) chromosome is a modified abnormal 10 deficient for the W2 and Sr2 loci as well as the large K10 knob and the euchromatic tail. It is female and male transmissible albeit with a somewhat reduced male frequency. Homozygotes for DfK10(F) have defective endosperm development and produce white seedlings--i.e., the homozygous deficiency has the same phenotype as the w2 mutation. The DfK10(F)/w2 compound behaves exactly the same as the DfK10(F)/DfK10(F) and the w2/w2 homozygotes. Since the known deficiency in 1OL and the w2 mutation give identical phenotypes, the possibility that the original w2 mutation is a deficiency including more than one gene should be considered.
Homozygous DfK10(F), homozygous w2, and heterozygous DfK10(F)/w2 kernels all exhibit a third mutant trait. In kernels possessing only dominant alleles for the complementary loci concerned with aleurone color, the aleurone layer is not uniformly pigmented but has a spotted appearance resulting from the interspersion of numerous islands of colorless cells among pigmented sectors. The colorless areas or spots coincide with the depressed regions of defective endosperm, while the normally developed sectors are colored. The spotted phenotype, first observed in DfK10(F) R -/N10 r w2 heterozygotes, simulated a mutable R system, but this explanation became untenable when we found that the spotted phenotype also occurred in R w2 and DfK10(F) R - homozygotes. Aleurone cells were present in the defective colorless regions of the endosperm so the lack of pigment cannot be ascribed to a missing aleurone layer. We think it likely that the failure to form anthocyanin in the depressed areas of the endosperm is caused by pigment inhibition resulting from the loss or mutation of a gene in the w2 region. Suppression of pigment synthesis in DfK10(F) or w2 homozygotes is comparable to the action of the recessive vp mutation, which likewise inhibits anthocyanin production in cells possessing all of the genes necessary for aleurone color. In summary, the three apparently unrelated phenotypic effects produced by homozygosity or hemizygosity for w2 are found when the DfK10(F) R - chromosome, known to be deficient for the W2 gene is homozygous. These observations suggest that three closely linked but separate loci were lost when the W2 mutation arose, but pleiotropy of a single gene cannot be excluded and remains a viable alternative. Since some small deficiencies, such as Stadler's a-x mutations, are known to reduce crossing over in flanking regions, we thought it might be informative to determine the amount of recombination between R and Sr2 in plants heterozygous for w2 and in sib plants homozygous for the W2 allele, since these markers flank the w2 locus. In a population of 935 individuals heterozygous for w2, we found 32.8% recombination between R and Sr2, and 11.3% for the proximal G R region. Among 481 W2/W2 control plants, The R Sr2 recombination was 28.7% and the G R recombination 11.6%. Admittedly, the data are not extensive but should reveal a marked reduction in crossing over if the w2 mutation is a segmental deficiency. Since no reduction was found for the critical R sr2 region, which includes the w2 locus, it can only be concluded that the reombination data offer no support for the hypothesis that the w2 mutation is associated with a deficiency.
M. M. Rhoades and E. Dempsey
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