Abstract
PK23-2, a line of six-rowed barley (Hordeum vulgare L.) originating from Pakistan, has resistance to Japanese strains I and III of the barley yellow mosaic virus (BaYMV). To identify the source of resistance in this line, reciprocal crosses were made between the susceptible cultivar Daisen-gold and PK23-2. Genetic analyses in the F1 generation, F2 generation, and a doubled haploid population (DH45) derived from the F1 revealed that PK23-2 harbors one dominant and one recessive resistance genes. A linkage map was constructed using 61 lines of DH45 and 127 DNA markers; this map covered 1268.8 cM in 10 linkage groups. One QTL having a LOD score of 4.07 and explaining 26.8% of the phenotypic variance explained (PVE) for resistance to BaYMV was detected at DNA marker ABG070 on chromosome 3H. Another QTL having a LOD score of 3.53 and PVE of 27.2% was located at marker Bmag0490 on chromosome 4H. The resistance gene on chromosome 3H, here named Rym17, showed dominant inheritance, whereas the gene on chromosome 4H, here named rym18, showed recessive inheritance in F1 populations derived from crosses between several resistant lines of DH45 and Daisen-gold. The BaYMV recessive resistance genes rym1, rym3, and rym5, found in Japanese barley germplasm, were not allelic to rym18. These results revealed that PK23-2 harbors two previously unidentified resistance genes, Rym17 on 3H and rym18 on 4H; Rym17 is the first dominant BaYMV resistance gene to be identified in primary gene pool. These new genes, particularly dominant Rym17, represent a potentially valuable genetic resource against BaYMV disease.
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This work was conducted by the malting barley breeding program in Fukuoka Agricultural Research Center, and supported by a Grant-in-Aid from the Ministry of Agriculture, Forestry and Fisheries of Japan.
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Communicated by A. Graner.
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Kai, H., Takata, K., Tsukazaki, M. et al. Molecular mapping of Rym17, a dominant and rym18 a recessive barley yellow mosaic virus (BaYMV) resistance genes derived from Hordeum vulgare L.. Theor Appl Genet 124, 577–583 (2012). https://doi.org/10.1007/s00122-011-1730-5
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DOI: https://doi.org/10.1007/s00122-011-1730-5