The complex nature of the Rp1 rust resistance locus allows certain combinations of Rp1 genes to be recombined into the cis configuration (Saxena and Hooker, P.N.A.S. 61:1300, 1968; Hu and Hulbert, Genome 37:742, 1994). We have constructed a number of different recombinants carrying two or three tightly linked Rp genes. Such 'compound' Rp1 genes can now be manipulated together as single genes. Two different recombinants (Rp1-DJ4 and Rp1-DJ46) were identified which carried both Rp1-J and Rp1-D. Progeny from these recombinants, which were segregating for the compound genes, also segregated for a mild lesion-mimic phenotype. None of the parental lines showed the phenotype. In addition, all of the plants in the segregating families with noticeable necrotic or chlorotic spots carried the compound gene. Several lesion-mimics have previously been identified which are thought to have resulted from mutation or recombination events at Rp1 (Pryor, TIG 3:157, 1987; Hu et al. unpublished). It is, therefore, possible that certain combinations of 'wild type' Rp1 genes may contribute to a lesion-mimic phenotype. The experiment reported here was meant to determine the relationship between the Rp1-DJ resistances and the lesion-mimic phenotype.
The Rp1-DJ46 and Rp1-DJ4 compound genes were crossed twice to three inbred lines, H95, A188 and W23. Plants carrying the Rp1 genes were then self-fertilized and the resulting BC1 F2 families were planted in the field. Individual plants in each family were self-fertilized, at which time they were rated for lesion mimic phenotypes. Ratings for individual plants are based on the percentage of leaf area on the lower leaves that was covered by chlorotic or necrotic spots (Table 1); for instance, '0' indicates no spots and '2' indicates 20% of the area of the lower leaves was covered by lesions. The Rp1 genotypes of the individual plants were subsequently determined by progeny testing. Plants designated 'RR' or 'Rr' in Table 1 carry the compound gene while those designated 'rr' are homozygous for the rp1 allele of the recurrent parent.
Table 1. Distribution and severity of lesion-mimic phenotypes in BC1F2
families segregating for Rp1-J + Rp1-D recombinants
in different genetic backgrounds.
|8||1 Rr||1 RR||----||4 Rr||2 RR|
|7||1 RR||---||----||1 Rr||1 RR, 1Rr|
|6||1 Rr||2 RR||----||---||1 Rr|
|5||1 RR||---||----||1 Rr, 1rr||1 Rr|
|4||3 Rr||1 Rr||1 Rr||1 rr||1 Rr, 1 rr|
|3||2RR,2Rr||1 Rr||2 Rr||---||1RR,1Rr,1rr|
|2||2 Rr, 2rr||1 Rr||2 Rr||2 rr||2RR,4Rr,1rr|
|1||1 Rr, 1rr||6 Rr, 1 rr||3 RR,1Rr,2rr||---||---|
|0||4 Rr, 4rr||1RR,6Rr,1rr||2RR,4Rr,2rr||2 rr||4Rr,3rr|
Examination of the data reveals two points. First, there is an apparent correlation between the Rp1-DJ compound gene and a lesion-mimic phenotype. In the A188 and H95 backgrounds, 28 out of a total of 96 plants were rated as '6' or higher and all these carried the Rp1-DJ compound gene. Second, the expression of the phenotype is dependent on other genetic factors besides Rp1. This is indicated by individuals that carry the Rp1 compound gene but do not show the phenotype in each of the families. It is also apparent when comparing the severity of phenotypes in the different genetic backgrounds. The expression of the lesion-mimic phenotype is very weak in the W23 background as compared to the A188 or H95 background.
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