RFLP mapping of maize mosaic virus resistance gene
--R. Ming, M.D. McMullen, J.L. Brewbaker, R.C. Pratt, H.G. Moon, T.
Musket, and D.T. Kyetere
Maize mosaic virus (MMV), transmitted by the leafhopper Peregrinus maidis (Ashmead), causes a common disease of maize in many tropical and subtropical countries. Ninety-one recombinant inbred lines (RILs), derived from the cross Hi31 (a B68 conversion) and Ki14 (a Thai inbred), were used for MMV resistance gene mapping. Previously, a resistance gene in Hi31, tracing back to Caribbean flints (Brewbaker and Aquilizan, Crop Sci. 5:412-415, 1965), was identified and named Mv (Brewbaker, Ohio So. Coop. Series Bull. 247:145-151, 1981). The RILs were screened for the disease under a natural infection in Hawaii in the summer of 1994 in a field where susceptible corn was planted successively for a year to increase the virus. The first 10 plants from each line were rated for disease response in two replications using a 1-9 scale (1=no symptom, 9=severe symptom). Twenty sub-lines each were grown of resistant parent Hi31 (mean 1.10, range 1.0 to 2.0)and susceptible parent Ki14 (mean 6.15, range 5.0 to 7.0). The disease rating for the RILs ranged from 1.0 to 7.0.
Based on the phenotypic scores, 28 highly susceptible RILs were chosen for the pooled-sampling approach. DNA from the parents, RILs, and the susceptible pool was digested by eight restriction enzymes: EcoRI, HindIII, EcoRV, BamHI, DraI, XbaI, BglII and SacI. One hundred sixty-three DNA probes distributed throughout the 10 chromosomes of maize were used to screen parents and the susceptible pool. One hundred fourteen informative probes were used for analysis of the RILs. Since duplicated loci were exhibited from 13 probes, a total of 127 loci were genotyped for these RILs.
Initial evidence for the Mv map position was obtained from the pooled-sampling approach, as probes on chromosome 3 near the centromere were biased to the susceptible parent allele. The SAS/GLM procedure was used to determine the correlations between RFLP markers and the MMV resistance (Table 1).
Table 1. The loci significantly associated with MMV resistance from
single factor analysis of variance.
| Marker | Chrom. | Position* | R^2 | Probabil. |
| umc121 | 3 | 18 | 0.0615 | 0.0206 |
| csu16 | 3 | 40 | 0.1983 | 0.0031 |
| php20042 | 3 | 45 | 0.2409 | 0.0020 |
| umc102 | 3 | 78 | 0.3202 | 0.0001 |
| csu30 | 3 | 83 | 0.3768 | 0.0001 |
| php20508 | 3 | 84 ** | 0.4169 | 0.0001 |
| umc26 | 3 | 86 | 0.4014 | 0.0001 |
| bnl5.37 | 3 | 98 | 0.1491 | 0.0003 |
Loci on chromosome 3 near the centromere (umc102, csu30, php20508, umc26) showed the greatest effects, indicating a major MMV resistance gene was located in this region. This gene is present in the resistant parent Hi31 and apparently traces back to the Argentine parent used in conferring common rust resistance into B14. The results confirmed Brewbaker's suggestion from near-isogenic conversions that mv is linked to lg2 and na1 on chromosome 3 (Brewbaker, Proc. Annu. Corn Sorghum Res. Conf. 29:118-133, 1974). A number of RFLP probes on chromosomes 4, 7, and 9 were marginally significant for MMV resistance. Possible QTLs for MMV resistance on these chromosomes will need to be confirmed with larger populations.
We conclude that resistance to MMV in B68 and Caribbean flints involves a major QTL on chromosome 3 linked to RFLP marker php20508. This gene is probably the previously described gene mv.
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