Phenotyping And Genotyping Powdery Mildew Resistance In Pea

Pea powdery mildew caused by Erysiphe pisi DC. is an important pea disease. The conidia of thispathogen spread by air flow, leading to a large-scale disease epidemic. This disease can cause25%-50%yield losses in the main pea producing areas. At present, the main method to controlpowdery mildew is earlier sowing or planting resistant cultivars. In addition, chemical method is alsoan effective way. But extensive use of fungicides will cause environmental and food safety issues, andmay also lead to fungicide-resistant mutant of the pathogen. Therefore, the use of resistant varieties isthe most effective and economic way to control powdery mildew and improve quality and yield. Upto date, only three powdery mildew resistance genes have been identified, two single recessive genes,er1and er2in pea, and one dominant gene Er3in wild pea. Therefore, it is more urgent to find newresistance alleles to prevent the powdery mildew. In this study,(1) identify and evaluate the resistanceof domestic and foreign pea cultivars to powdery mildew;(2) identify the genotype of Canadianaccessions using the markers linking to er1;(3) analysis homologous PsMLO1gene sequence in3peacultivras immune to powdery mildew,(4) map a new er1allele in landrace G1778.1.111F5lines derived from X9002×S3008were evaluated resistance to powdery mildew isolateEPBJ in seedling stage. The results showed that27pea lines were resistant to powdery mildew,51pea lines were heterozygous to powdery mildew,33pea lines were susceptible to powdery mildew.The segregation ratio of resistant and susceptible plants in45pea lines fits with the genetic model of1:3ratio which showed that the resistance of X9002to powdery mildew could be controlled by onerecessive gene.2.403pea accessions from China and other countries were evaluated resistance to the Beijing andYunnan powdery mildew isolates in seedling stage. The results showed that32and43accessionswere immune to EPBJ and EPYN, respectively, and33and32accessions were resistant to EPJB andEPYN, respectively. In addition,28accessions were both immune to EPBJ and EPYN, while13accessions were both resistant to EPJB and EPYN. The results indicated that there were richresistance sources in the pea germplasm.3. A、B、C、D and E marker genotypes have been identified in36selected accessions with fourSCAR makers closely linked to pea powdery mildew resistance gene er1, which included24,7,1,3and1cultivars (lines), respectively. The main marker genotype was A marker genotype.4. cDNA sequences homologous to PsMLO1were obtained in cultivars Tara and Cooper fromCanada and landrace G1778from Yunnan, the length of which was1677bp,1749bp and1786bp,respectively. The homology with PsMLO1of the three cDNA sequences was99%by the BLASTnanalysis in NCBI. The homologous sequences of PsMLO1in Cooper and Tara both have a pointmutation (ie, C�'G) in the680bp which lead to a stop codon (UGA), so that the protein synthesis are early terminated. This kind of mutation belongs to the allele er1-1. The point mutation occurred at1121bp (ie T�'C) in the sequence of G1778, belonging to a new allele of er1and change leucine intoproline at the first391amino acids of PsMLO.5. G1778was used as female parent to cross with the susceptible Bawan6, and F2and F3generations were obtained by self-crossing. By artificial inoculation, F1plants were susceptible topowdery mildew, and the resistant and susceptible segregation ratio in71F2plants fit well with agenetic mode of1:3ratio, which revealed that the resistance in G17789was controlled by a recessivegene. Resistance gene in G1778was identified and mapped using the molecular markers. Theresistance gene in G1778was located to the molecular linkage group VI based a linkage SSR markerAD60. A gene marker c5DNAmet in the LG VI also linked to the resistance gene c5DNAmet andAD60have a genetic distance of24.8cM and8.8cM to the resistance gene, respectively. Based onthe results of the PsMLO1gene sequence analysis and the molecular mapping, the resistance gene topowdery mildew in G1778is a new allele in er1locus, which was named er1-6.