Cg and Tp2 are gain-of-function mutations

The nature of a mutation can often be deduced by varying the dosage of the normal allele of the gene. A mutation that reduces the level of a gene product (i.e., a hypomorphic or null mutation) should, at least in theory, be phenotypically corrected by a duplication of the normal allele, whereas the phenotype of a gain-of-function mutation will either be accentuated or only partially corrected by a duplication.

In order to create plants carrying duplications of the normal alleles of Cg and Tp2, stocks homozygous for these mutations were crossed as female by B-A translocation stocks. The Tp2 stock used in this study was homozygous for g and r-g and was crossed by TB-1OLa and TB-10L19 G R-scm stocks. Hyperploids were identified as kernels having a colored embryo and colorless endosperm; as expected, all such kernels gave G seedlings. Because Cg was not linked to a recessive marker, hyperploids from the cross Cg x TB-3Sb were identified by chromosome number. In both instances hyperploid individuals were clearly mutant in phenotype. In fact, none of the progeny from these crosses were completely normal. This result strongly suggests that Cg and Tp2 are not hypomorphic or null mutations, and therefore must involve a gain of function. Whether they are responsible for the overproduction of a normal gene product or the production of an antimorphic product will be examined by reversion studies, and by a more comprehensive dosage analysis.

R. S. Poethig


Please Note: Notes submitted to the Maize Genetics Cooperation Newsletter may be cited only with consent of the authors.

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