1. Locating genetic factors for kernel‑row number by use of translocations.

 

This study was undertaken to obtain experimental evidence on the number and location of genes affecting kernel‑row number in maize.

 

Four different twelve‑rowed maize inbreds were crossed to a series of eight‑rowed lines, each of which was heterozygous for one of various well‑distributed translocations. Some of the semisterile segregates (translocation heterozygotes) in the F1 generation were backcrossed to their twelve‑rowed parent and an equal number was crossed to the nornal eight‑rowed inbred R. The progeny of the F1's backcrossed to the twelve‑rowed parent and those crossed to the eightrowed inbred were grown and classified for row number and semisterility.

 

Analyses of variance, based on the means for kernel‑row number in the normal and semisterile segregates of each culture, were calculated for each group of segregates having a common twelve‑row parent. Significant or highly significant differences between replications were found in each of the analyses. Thus, it was concluded that environment may play a greater role in affecting the expression of the number of kernel rows of the maize plant than was formerly believed.

 

Each analysis of variance showed that there were highly significant differences in the mean kernel‑row number of the lines derived from the various eight‑row translocation lines. It was concluded that lines of the same eight‑row phenotype may be of different row‑number genotypes.

 

As was expected, the progeny of the lines which had been backcrossed to the twelve‑rowed parent had a higher mean kernel‑row number than the progeny of the lines crossed to the eight‑rowed inbred.

 

The frequency distributions for number of kernel rows of the semisterile plants were compared with those of their normal sibs in an attempt to find evidence of linkage between genes for kernel-row number and the translocation loci.

 

Summarizing the linkage evidence and interpretations on dominance the following conclusions were drawn concerning the genes that differentiate the eight‑ from the twelve‑rowed condition in each of the twelve‑rowed lines.

 

The twelve‑rowed line 39 differs genetically from the eight-rowed condition by the following genes:

 

a. Two or more genes lacking dominance, or two or more groups of dominant + and ‑ genes closely linked in the repulsion phase. One of these genes or groups of genes is located near the P locus in chromosome 1. The other gene or group of genes is located in the long arm of chromosome 1 or the long arm of chromosome 7, or both.

 

b. Two or more dominate genes for increasing kernel‑row number in the twelve‑rowed parent. One gene or group of genes is located in chromosome 3 near the ts4 locus. The other gene or group of genes is located in the short arm of chromosome 6 or in the long arm of chromosome 10, or both.

 

The twelve‑rowed line 2 differs genetically from the eight-rowed condition by the following genes:

 

a. A gene or genes lacking dominance or a group of dominant + and genes closely linked in the repulsion phase, located in chromosome 6 near the Y locus.

 

b. A dominate gene or genes for decreasing row number in the eight-rowed parent, located in chromosome 9 near the wx locus.

 

The twelve‑rowed line II differs genetically from the eight-rowed condition by a gene or genes lacking dominance or by a group of dominant + and ‑ genes linked in the repulsion phase, located in the long arm of chromosome 4 or the long arm of chromosome 6, or both.

 

The twelve‑rowed line 4 differs genetically from the eight-rowed condition by the following genes: two or more genes lacking dominance, or two or more groups of dominant + and ‑ genes closely linked in the repulsion phase. One gene or group of genes is located in chromosome 6 near the Y locus. The other gene or group of genes is located in the short arm of chromosome 2 or the long arm of chromosome 4 or both.

 

Other genes influencing kernel‑row number may well have gone undetected, since in these experiments all regions of the chromosomes were not adequately tested.

 

T. J. Mann