C-I-m836976 arose by the insertion of a mobile element into the C-I allele in a population of C-I/C-I En, En, (En?). This allele was one of several unstable C-I alleles (MGCNL 58:2) uncovered in this population. When in combination C-I-m/C, the phenotype is colored, mutating to colorless. The C-I-m allele has not been seen as a homozygote and thus it is not known whether it is C-m or c-m. What is clear is that it mutates to C-I, as is evident in the colorless sectors of the C-I-m/C heterozygote. In the cross of c2-m2 wx-m8 x C-I-m Sh Bz Wx/C sh bz wx; En, En (Cross A), the following progeny were observed in a small sample from two ears:
The following comments can be made on this small sample. The wx --> Wx phenotype is from En acting on the wx-m8 allele originating from the female parent in the heterozygote, wx/wx-m8. En came from the C-I parent. Thus the excess wx --> Wx kernels among the full colored - not sectored class must be caused by many En rather than a linked En. The kernels that are sectored and wx -->Wx are from cross-overs.
There is an excess of sectored in ear 2. This is not explainable in view of the observation of the expected Wx vs. wx ratios in ear 1 and ear 2.
The absence of kernels that are sectored and waxy and the presence of full colored and waxy is strong support that sectoring is strongly correlated with the En effect on the wx-m8 allele. It is not possible to conclude on the state of En at the C-I-m allele since the additional En in the material does not allow a more definitive answer. It can, however, be concluded that the C-I-m allele sectoring is En-dependent.
There is a possible explanation for the C-I allele mutation event. It appears that the original C-I is caused by a stable insert (MGCNL 58:2) that becomes part of a chimeric transcript and the resulting protein is consequently distorted (Peterson and Leleji, Canad. J. Genet. Cytol.). For C-I-m836976, En or I was inserted in such a manner to inhibit the locus such as typical c-m(r) or a2-m(r). By excision of I, the original locus condition is restored and capable of inhibiting anthocyanin formation.
Peter A. Peterson
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