Kansas State University
Recombination between Rp1-G and Rp5
--M.A. Sudupak, K.S. Hong and S.H. Hulbert
Race specific resistance to the fungal pathogen Puccinia sorghi occurs at 6 or 7 identified loci in maize. Many of the resistance factors identified, however, map to one of these loci. At least 14 different resistance factors, Rp1-A - Rp1-N, were mapped to the Rp1 locus on the short arm of chromosome 10 by Hooker and co-workers. Each allele has a distinct response to different races of Puccinia sorghi. The Rp1 locus is flanked by the RFLP markers bnl3.04 on the distal side and npi422 and npi285 on the proximal side. Recombinational analyses of Rp1 using flanking RFLP markers has indicated that most of the Rp1 alleles are clustered closely together (within 0.5cM) but the Rp1-G gene maps one to three map units distally, depending on the cross (MGG 226:377). Rp5 also mapped about three map units distally.
In order to determine the recombinational relationship between Rp1-G and Rp5, we constructed testcross populations segregating for both genes. Rp1-G R168 was crossed to Rp5 R168 and the F1 was crossed to the susceptible inbreds Oh43 and H95. These populations were then screened for susceptible individuals using the rust isolate IN1 which is avirulent on both Rp1-G and Rp5 (Plant Dis. 75:1130-). Three susceptible recombinants were observed in 3450 seedlings. The distal RFLP marker, bnl3.04 was not informative in this cross, so it could not be verified that the susceptible progeny were derived by crossing over between Rp1-G and Rp5. However, virtually all of the susceptible progeny we have isolated from other Rp1 heterozygotes have had nonparental combinations of flanking markers. The proximal marker, npi285, was informative in this cross and all three susceptible progeny had the Rp1-G parent allele, as would be expected if Rp1-G maps distally to Rp5. These data, however, should be interpreted with caution; we have observed both types of nonparental flanking markers in testcrosses of certain Rp1 heterozygotes, presumably due to mispairing of duplicated sequences and crossing-over. It is therefore possible that when more Rp1-G-Rp5 recombinants are analyzed the other flanking marker configuration will be observed. Furthermore, the observed frequency of recombination between Rp1-G and Rp5 is about eight times lower than the frequency of instability of Rp1-G homozygotes observed by Pryor (MNL 61:37) and we have not yet determined the mechanism causing instability of Rp1-G.
The distal position of Rp1-G has indicated that Rp1-G maps to a locus separate from the other Rp1 alleles and it appears to be either allelic to, or distal to, Rp5. Like the other Rp1 area genes tested so far, Rp1-G is proximal to the closely flanking RFLP locus bnl3.04. When 130 random test cross progeny from the cross (Rp1-G R168 X Rp1-I R168) X B14 were scored for rust resistance and bnl3.04 genotype, two recombinants were observed between Rp1-G and bnl3.04. Two other progeny were recombinant between Rp1-I and Rp1-G indicating that Rp1-G maps between Rp1-I and bnl3.04.
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