Molecular mapping of pea powdery mildew resistance gene <Emphasis Type="Italic">er2</Emphasis> to pea linkage group III |
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Authors: | V Katoch Susheel Sharma S Pathania D K Banayal S K Sharma R Rathour |
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Institution: | (1) Hill Agricultural Research and Extension Center, H.P. Agricultural University, Kukumseri, Himachal Pradesh, 175142, India;(2) Department of Plant Pathology, H.P. Agricultural University, Palampur, Himachal Pradesh, 176062, India;(3) Department of Agricultural Biotechnology, H.P. Agricultural University, Palampur, Himachal Pradesh, 176062, India; |
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Abstract: | Powdery mildew caused by Erysiphe pisi D.C. is one of the most serious diseases that inflict heavy losses to pea crop world-wide. Identification of resistance sources
and their incorporation into susceptible cultivars remains the most effective method of controlling the disease. The present
study investigated the resistance phenotype, inheritance, and genomic location of gene(s) controlling resistance to powdery
mildew in pea genotype ‘JI2480’. The powdery mildew resistance in ‘JI2480’ appeared to be a spatial phenomenon showing expression
only in leaf tissues. By segregation analysis of an F2 progeny of cross ‘Lincoln/JI2480’, the leaf resistance of ‘JI2480’ was shown to be controlled by a single recessive gene,
presumed to be er2. Through linkage analysis of 111 resistant F2 progeny plants with simple sequence repeat (SSR) and random amplified polymorphic DNA (RAPD) markers adopted from the published
linkage maps, the er2 gene was localized on pea linkage group III (LGIII). The assignment of er2 to LGIII, a position different from that reported for er1, has resolved the long standing controversy in the literature regarding the existence and genomic location of er2 gene. A RAPD marker OPX-17_1400, exhibiting cis phase linkage (2.6 cM) to er2 was successfully converted to a sequence characterized amplified region (SCAR) marker, ScX17_1400. The SCAR marker ScX17_1400
will ensure speedy and precise introgression of er2 into susceptible cultivars by permitting selection of er2 heterozygotes amongst BC
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F1s without progeny tests and resistance screening. |
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