The Tunicate mutation causes glumes in the ear and tassel to become abnormally large. Mangelsdorf and Galinat (PNAS 51:147-150) demonstrated that this mutation has 2 components, both of which have a weak Tu phenotype, and that these components can recombine to reconstitute a mutation having the severe phenotype of the original locus. This observation raises the possiblity that Tu is a duplication, and that its phenotype is a result of the overproduction of the product encoded by this locus. To test this hypothesis, Tu c2/+ c2 plants were crossed by TB-4L, and plants of the genotypes Tu/+/+ , Tu/-, were identified on the basis of the expression of c2 in the endosperm. Seeds having colorless endosperms were assumed to have hyperploid embryos, those with pale purple endosperms were assumed to have diploid embryos, and those with dark purple endosperms were assumed to have hypoploid embryos. The hypoploid nature of the latter class of seeds was confirmed by the fact that they produced small, weak plants.

All 3 classes of plants had a Tu phenotype, although hypoploids were more severely affected than either diploid or hyperploid plants. The fact that Tu is expressed in hyperploids (Tu/+/+) indicates that this mutation reflects a gain-of-function rather than a loss-of-function, because a loss-of-function would have been compensated by the 2 wild type alleles in these plants. If this gain-of-function involved the overproduction of a wild type product, as would be expected of a duplication, hypoploid plants (Tu/-) should have a less severe Tu phenotype than their diploid or hyperploid siblings. This was not the case. The fact that wild type alleles reduce the expression of Tu (relative to the hypoploid condition) suggests that Tu may encode a product that antagonizes normal gene activity, but other alternatives cannot be excluded.

Scott Poethig
 
 

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