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Characterisation of the late blight resistance in potato differential MaR9 reveals a qualitative resistance gene, R9a, residing in a cluster of Tm-2 2 homologs on chromosome IX

Late blight of potato (Solanum tuberosum), caused by Phytophthora infestans, can effectively be managed by genetic resistance. The MaR9 differential plant provides durable resistance to a broad spectrum of late blight strains. This resistance is brought about by at least seven genes derived from S. demissum including R1, Rpi-abpt1, R3a, R3b, R4, R8 and, so far uncharacterized resistance gene(s).

Kwang-Ryong Jo, Richard G. F. Visser, Evert Jacobsen, Jack H. Vossen

Theoretical and Applied Genetics May 2015, Volume 128, Issue 5, pp 931-941

Abstract

Key message

The durable late blight resistance in potato plant Ma R9 is genetically characterized. A novel R -gene is mapped. The monogenic nature and map positions of R9 are negated and rectified.

Abstract

Late blight of potato (Solanum tuberosum), caused by Phytophthora infestans, can effectively be managed by genetic resistance. The MaR9 differential plant provides durable resistance to a broad spectrum of late blight strains. This resistance is brought about by at least seven genes derived from S. demissum including R1, Rpi-abpt1, R3a, R3b, R4, R8 and, so far uncharacterized resistance gene(s). Here we set out to genetically characterize this additional resistance in MaR9. Three BC1 populations derived from MaR9 were identified that segregated for IPO-C resistance but that lacked R8. One BC1 population showed a continuous scale of resistance phenotypes, suggesting that multiple quantitative resistance genes were segregating. In two other BC1 populations resistance and susceptibility were segregating in a 1:1 ratio, suggesting a single qualitative resistance gene (R9a). A chromosome IX PCR marker, 184-81, fully co-segregated with R9a. The map position of R9a on the distal end of the lower arm of chromosome IX was confirmed using PCR markers GP101 and Stm1021. Successively, cluster-directed profiling (CDP) was carried out, revealing six closely linked markers. CDPSw58, CDPSw59 and CDPSw510 flanked the R9a gene at the distal end (5.8 cM) and, as expected, were highly homologous to Sw-5. CDPTm22 flanked R9a on the proximal side (2.9 cM). CDPTm26 and CDPTm27 fully co-segregated with resistance and had high homology to Tm-2 2 , showing that R9a resides in a cluster of NBS–LRR genes with homology to Tm-2 2 . Besides R9a, additional resistance of quantitative nature is found in MaR9, which remains to be genetically characterized.

 

See http://link.springer.com/article/10.1007/s00122-015-2480-6

 

 

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