Discovery of a Novel er1 Allele Conferring Powdery Mildew Resistance in Chinese Pea (Pisum sativum L.) Landraces

Abstract

Pea powdery mildew, caused by Erysiphe pisi D.C., is an important disease worldwide. Deployment of resistant varieties is the main way to control this disease. This study aimed to screen Chinese pea (Pisum sativum L.) landraces resistant to E. pisi, and to characterize the resistance gene(s) at the er1 locus in the resistant landraces, and to develop functional marker(s) specific to the novel er1 allele. The 322 landraces showed different resistance levels. Among them, 12 (3.73%), 4 (1.24%) and 17 (5.28%) landraces showed immunity, high resistance and resistance to E. pisi, respectively. The other landraces appeared susceptible or highly susceptible to E. pisi. Most of the immune and highly resistant landraces were collected from Yunnan province. To characterize the resistance gene at the er1 locus, cDNA sequences of PsMLO1 gene were determined in 12 immune and four highly resistant accessions. The cDNAs of PsMLO1 from the immune landrace G0005576 produced three distinct transcripts, characterized by a 129-bp deletion, and 155-bp and 220-bp insertions, which were consistent with those of er1-2 allele. The PsMLO1 cDNAs in the other 15 resistant landraces produced identical transcripts, which had a new point mutation (T→C) at position 1121 of PsMLO1, indicating a novel er1 allele, designated as er1-6. This mutation caused a leucine to proline change in the amino acid sequence. Subsequently, the resistance allele er1-6 in landrace G0001778 was confirmed by resistance inheritance analysis and genetic mapping on the region of the er1 locus using populations derived from G0001778 × Bawan 6. Finally, a functional marker specific to er1-6, SNP1121, was developed using the high-resolution melting technique, which could be used in pea breeding via marker-assisted selection. The results described here provide valuable genetic information for Chinese pea landraces and a powerful tool for pea breeders.

Two Novel er1 Alleles Conferring Powdery Mildew (Erysiphe pisi) Resistance Identified in a Worldwide Collection of Pea (Pisum sativum L.) Germplasms

“…This mutation differed from all known er1 alleles, indicating that the E. pisi resistance of G0004389 was controlled by a novel allele of er1 . This novel allele was designated er1 -8, following the accepted nomenclature [14,26,27,42,44,51]. In pea germplasm G0004400, a 1-bp deletion (T) was identified in a previously unreported position homologous to position 928 in exon 10 of the PsMLO1 cDNA sequence.…”

“…Their results have indicated that resistance to E. pisi is controlled by two single recessive genes ( er1 and er2 ) and one dominant gene ( Er3 ) [11,12,13,14]. The er1 , er2 , and Er3 genes have been mapped using linked markers [15,16,17,18,19,20,21,22,23,24,25,26,27]. The genes er1 and er2 map to pea linkage groups (LGs) VI and III, respectively [17,28].…”

“…To date, nine er1 alleles resistant to E. pisi have been identified in E. pisi -resistant pea germplasms: er1 -1 (also known as er1mut1 ) [14,21,25,40,41], er1 -2 [14,24,25], er1 -3 [14], er1 -4 [14], er1 -5 [38], er1 -6 [27], er1 -7 [26], er1 -10 (also known as er1mut2 ) [21,40,42], and er1 -11 [42,43]. Each er1 allele corresponds to a different PsMLO1 mutation site and pattern.…”

“…Among the nine er1 alleles identified, only er1 -1 and er1 -2 are commonly applied in pea breeding programs [14,38]. Several studies have attempted to design functional markers of er1 alleles to allow for the rapid selection of pea germplasms resistant to E. pisi [24,26,27,38,42,43,44].…”

“…Several studies have focused on the identification of Chinese pea germplasms resistant to E. pisi [41,44,45,46,47,48,49]. In the Chinese pea cultivars X9002 and Xucai 1, E. pisi resistance is conferred by the er1 -2 allele [24,25,47], while in some Chinese pea landraces from Yunnan Province, E. pisi resistance is conferred by the er1 -6 allele [27,48]. E. pisi resistance in the Indian pea cultivar DDR11 is conferred by the er1 -7 allele [26].…”