| Maize dwarf mosaic(MDM) is one of the devastating and widespread viral diseases in the world.The most effective way to control the disease is to breed and popularize resistant hybrids based on screenings of resistant materials and understanding on the inheridity of resistance.In our previous study,one inbred line Siyi with elite agronomy traits was singled out and its inheritance of resistance to SCMV was studied.The results showed that two dominant complementary genes were detected to determine the resistance to sugarcane mosaic virus.The two genes were mapped on chromosome 3 and chromosome 6,respectively using microsatellite markers. The resistant gene RSCMV2 on chromosome 3 was flanked by SSR markers umc1527 and phi053 with the genetic distances of 1.8 and 2.1 cM respectively;whereas the resistance gene RSCMV1 on chromosome 6 was flanked by SSR markers umc2311 and bnlg1371 with the genetic distances of 2.1 and 1.5 cM.In addition,we found that different resistant individuals with different gene numbers displayed different phenotypes in the development of symptoms when infected with sugarcane mosaic virus in the F2 and BC1 population of Siyi×Mo17.This result indicates that the resistance to SCMV is likely to be controlled by the interaction of the two genes.Due to the complicated genetic background,the F2 population is not suitable for further analysing the action mode and fine mapping of the two dominant complementary genes.In this study,a set of NILs were developed using Mo17 and Siyi as a recurrent parent and current parent,respectively,and were used to conduct free mapping and analyze action modes of the two genes.The results were obtained as following:1.Fine mapping of RSCMV1.674 F2 individuals derived from Mo17AaBB were used to conduct fine mapping of the RSCMV1.The resistant gene RSCMV1 was flanked by SSR markers umc1018 and umc2311 with the genetic distances of 3.7 and 1.9cM,respectively.Totally 18 individual plants showed recombination between RSCMV1 and SSR markers,including 9 individual plants between RSCMV1 and umc1018,and 9 plants between RSCMV1 and umc2311.The physical distance between the two SSR markers is 6.83 MB.which contained 43 BACs.Based on these BACs'sequences,47 pairs of SSR primers were developed by SSR-HUNTER software.27 pairs of primers showed clear PCR bands in Siyi or Mo17 and the effiency of primers designed is 57.4%.Among them,12 pairs of primers exhibited polymorphisms between Siyi and Mo17,and the effiency is 25.5%.17 pairs of Insertion-deletion length polymorphism(ILP) primers were also developed,in which only 4 pairs of ILP primers showed polymorphisms,and the effiency is 23.5%.Consequently,co-segregation markers A16-7,A4-3,A4-2 and a3-1 were detected and RSCMV1 was further located in a 3.3×106 bp long region on chromosome 6.2.Fine mapping RSCMV2.The F2 individuals derived from Mo17AABb were used to conduct fine mapping of RSCMV2,and 30 pairs of primers showed polymorphisms between Siyi and Mo17. RSCMV2 was flanked by SSR markers umc1693 and bnlg1601 with the genetic distances of 1.7 and 0.9 cM,respectively.45 recombinated plants were found and were used for fine mapping and position cloning.3.Action mode analysis of two dominant complementary genes using NILs.Significant differences in response to SCMV were observed among a set of NILs with different numbers of resistance genes in the years of 2006 and 2007,respectively.The plants with two resistant genes showed complete resistance during whole growth stages,while other plants with single resistant gene are suspectible.The plants with the single gene RSCMV2 showed a typical diseased symptom at earlier stage about one week after inoculation,similar to the suspectible parent Mo17.The plants with the single gene RSCMV1 are suspectible,but it only displayed slight sympotom with 10 days later than Mo17.These results suggest that RSCMV1 is likely a predominant gene and shows basal resistance to SCMV,while RSCMV2 shows specific resistance at adult stage.
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