We reported unexpected results from our rhm tagging project, which indicated that there are two linked genes, designated rhm1 and rhm2, involved in chlorotic-lesion resistance to Bipolaris maydis (Chang and Peterson, MNL 68:4-6, 1994). We arbitrarily set the dominant gene in the T line as Rhm1 and that in the Cy line as Rhm2.
The two-gene model predicts that the inbred lines, which were shown (Smith and Hooker, Crop Sci. 13:330-331, 1973) to have a single, dominant gene for susceptibility to this disease have, in fact, two genes, with only one being dominant. The dominant gene in these inbred lines should recombine with one of the two dominant genes designated in this study, but not with both. A recombination test (Fig. 1) has been carried out to verify this prediction. Several inbred lines were selected from Smith and Hooker's study and crossed separately with our designated Rhm1 and Rhm2 lines and the F1's were testcrossed by the rhm tester. Summarized results from these tests are listed in Table 1.
As shown in Table 1, 5 (B14, B37, Oh51A, c2 W22 and a2 bt) of the 9 lines for which data are available clearly recombined with the T line while one (W64A) did not. The lack of recombination in one line and in some progeny families of others is an indication of heterozygosity of the original T line at the rhm2 (see later) locus rather than a paradox to our model, since the T line was developed originally by crossing two lines with different origins, followed by selfing for several generations. The results in Table 1 also clearly show that none of the tested lines recombined with the Cy line. This indicates that the inbred lines tested have the same dominant gene as the Cy line. Mo17 and B73 segregated with the Cy line. Tests of the original parent of B73 and one progeny family showed that our B73 line has a homozygous recessive genotype (rhm1 rhm2//rhm1 rhm2). A test of two progeny families showed that Mo17 has an array of genotypes at the rhm1 locus (see later).
Since the rhm gene originally identified by Smith and Hooker is often referred to as rhm1, we now designate the dominant gene in the Cy line as Rhm1 (rhm1 for a more generic term), which is the same as the originally identified rhm gene, and the dominant gene in the T line as Rhm2 (rhm2), which is a second gene involved in chlorotic-lesion resistance to B. maydis. Note that these designations are reversed from our last year's report (Chang and Peterson, MNL 68:5-6, 1994), to be consistent with the literature.
Figure 1. Test of the two-gene model, the recombination test. The Rhm1 gene in the inbred lines of Smith and Hooker's study should recombine with the Rhm gene either in the T line or in the Cy line, but not both. Consistency with this predicted result will indicate a questionable definition of the genotypes prior to the tests.
Table 1. Results of the recombination tests. Crossing scheme is shown
in Figure 1. Number of symbols (+, -, or seg., etc.) represents the number
of families showing the designated event. + Recombination seen; - No recombination;
seg. Segregation.
| Line | Cross with T line (Rhm2) | Cross with Cy line (Rhm1) |
| B14 | + - | - - - - |
| B37 | + + + - | - - - - |
| B73 | Data not available | seg. seg. seg. seg. |
| Mo17 | seg. + | seg. seg. seg. - |
| Oh51A | + + - - | - - - - |
| W64A | - - | - - |
| c2 W22 | + | - |
| a1-m(papu) | Data not available | - |
| a2bt | + | Data not available |
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