1ESALQ-Dept. of Plant Pathology, University of Sao Paulo, 13418-900 Piracicaba-SP, Brazil; 2Sementes Agroceres S.A., Dept. of Research, 13650-970 Sta. Cruz das Palmeiras-SP, Brazil

Background and objectives
The epidemiological profile of maize diseases in Brazil has dramatically changed after growers adopted the practice of the 'safrinha', or 'little crop', a second crop grown after the major one. Corn pathologists and breeders accept the tenet that this temporal expansion of the growing season caused an inoculum build up of several previously non-damaging pathogens. One such organism is Puccinia sorghi, the causal agent of common rust. Thus breeding for disease resistance against these pathogens became a major concern in Brazil. Although there are more than 25 known race-specific common rust resistance genes in maize, there is little information regarding the genomic position of partial quantitative resistance genes. Thus mapping efforts are currently under way in order to map quantitative resistance loci of maize to P. sorghi using microsatellite markers. The results presented here refer to a QRL identified on chromosome 2.

Materials and methods
The mapping strategy consisted of genotyping 97 F2 plants, derived from a cross between a resistant (L10) and susceptible (L20) inbred lines, with microsatellite marker-loci from chromosome 2 (bngl125, bngl381, bngl166, phi083, and bngl198), and evaluating their F3 progeny in the field. PCR amplification of microsatellite markers was done as described elsewhere [1], except that the final annealing temperature was 55C. Amplified fragments were resolved by electrophoresis on 3% agarose gels containing 0.5% ethidium bromide.

Two successive field trials were conducted at Agroceres' Experimental Station, in Santa Cruz das Palmeiras (Sao Paulo), in 1997. The experimental design consisted of a completely randomized block design with three replicates, with plots represented by 15 plants from each progeny grown as a single 2.5 m long row spaced 0.8 m apart. Parental lines and hybrid were included as control treatments. Plants were naturally infected and visual ratings of disease severity where taken from individual plants two to one week after flowering on a 0-9 severity scale in increments of 0.5, where 0=no symptoms and 9=more than 75% of leaf area affected by disease.

Analyses of variance were used to detect significant associations between each microsatellite marker locus and disease severity using the regression approach of the computer program STATISTICA (Statistica Inc., Tulsa, OK, USA). The percentage of the total phenotypic variance among genotypes at a given marker locus explained by the marker-trait association was estimated by the coefficient of determination R2. Linkage analyses among marker loci were done using MAPMAKER version 2.0.

Results and conclusions
Significant marker-trait loci associations (P=0.01) were found for markers bngl125, bngl381, bngl166, and phi083 in both trials, whereas locus bngl198 showed significant association only in trial 1. Coefficients of determination were higher in trial 1 perhaps due to the verified higher severity levels. Locus bngl125 explained the highest percentage of phenotypic variation in disease severity (R2=9%). All markers mapped to the same linkage group, covering 92 cM. The order of these markers was the same as on the maize consensus map for chromosome 2, but distances varied slightly. Since these markers are linked, it is assumed that they detect a single QRL. Taking bngl125 (located in bin 2.03) probably as the most closely marker linked to the resistance gene, the mode of gene action estimated for this QRL indicated that resistance was dominant. Moreover, alleles from the susceptible parent contributed towards greater resistance.

To the best of our knowledge, this is the first report of a QRL to P. sorghi located on chromosome 2, where resistance genes and QRL to other diseases and insects have been mapped, such as northern corn leaf blight, gray leaf spot, fusarium stalk rot, and European corn borer [2].

1. Chin ECL, Senior ML, Shu H, Smith JSC, 1996. Genome 39, 866-873.
2. McMullen MD, Simcox KD, 1995. MPMI 8, 811-815.