Additional loci for rust resistance
--Scot Hulbert and Jeff Drake
Common rust resistance genes have been mapped to three genomic regions in maize: The Rp1 area on 10S, which includes genes designated Rp5 and Rp6 and spans two or more cM; the Rp3 locus on chromosome 3, and the Rp4 locus on 4S. We have recently identified a gene from the hybrid 'Golden King' which segregates independently of these three areas.
Golden King was determined to carry two dominant genes for rust resistance (Hulbert et al. Plant Dis. 75:1130, 1991). One of these was phenotypically identical to Rp1-A and mapped to the Rp1 locus. The other provided resistance to a unique spectrum of rust pathotypes and segregated independently of the Rp1 genes. We have now determined that this gene also segregates independently of the Rp3 and Rp4 loci and propose the Rp7 designation. Test crosses of the following F1's with Rp7 segregated as two independent genes:
Rp3-F X Rp7 216:65 (res.:susc., pathotype KS1) X2 3:1
= 0.52, P > .25
Rp3-C X Rp7 141:52 (pathotype KS1) X2 3:1 = 0.39, P > .50
Rp4-B X Rp7 103:32 (pathotype OH1) X2 3:1 = 0.12, P > .50
An F2 family from the Rp4-B X Rp7 cross also segregated as expected for two dominant genes: 169 resistant: 8 susceptible to pathotype OH1; X2 15:1 = 0.90, P > .25. Since the Rp7 locus segregated independently of the Rp1, Rp3 and Rp4 loci, it represents a fourth locus controlling dominant resistance to common rust in maize.
The Rp7 gene confers high levels of resistance to ten of the 12 rust pathotypes in our collection. It does not provide resistance to pathotype HI1 from Hawaii, or KS2 from Kansas. In resistant reactions, most fungal infections result in small (usually < 1 mm) necrotic spots. Some limited sporulation occurs in some environments, and the pustules are usually surrounded by necrotic rings.
We have also identified a simply inherited resistance from the line CG13 which was obtained from A. L. Hooker's stocks at the University of Illinois. Preliminary analyses of crosses with this line have indicated a unique inheritance for this resistance. F2 progeny from the cross CG13 X H95 segregated 125 resistant:136 susceptible to rust pathotype IN1. The level of resistance in the resistant seedlings was very high, so scoring was unambiguous. Instead of the expected 3:1 or 1:3 ratios expected for single dominant or recessive genes, the segregation fit a 1:1 ratio (X2 = 0.46, P>.25). F3 families from 17 susceptible F2 individuals bred true for susceptibility. F3 families from eleven of the resistant F2 individuals all segregated for resistance. Analysis of an additional 23 random F3 families also failed to identify any that were homozygous resistant; eleven families were completely susceptible and 13 segregated for resistance. Segregation of resistance in F3 families was similar to that of the F2, closely fitting a 1:1 ratio. The combined ratio for 22 F3 families that segregated for resistance was 662:681 resistant: susceptible. Four of the resistant F2 plants were also backcrossed to the susceptible H95 parent. Each of these backcross families also segregated 1:1, resistant:susceptible (combined ratio = 132:140). The inheritance model we will test is that of a single locus where only the heterozygote confers resistance.
The resistance from the CG13 line is effective against only two of the rust pathotypes in our collection and is, therefore, unlikely to provide effective resistance in the field. It provides a very high level of resistance to pathotype IN1, and an intermediate level of resistance to IA1.
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