Selective genotyping to identify late blight resistance genes in an accession of the tomato wild species Solanum pimpinellifolium

Euphytica ◽  
2012 ◽  
Vol 187 (1) ◽  
pp. 63-75 ◽  
Author(s):  
Heather L. Merk ◽  
Hamid Ashrafi ◽  
Majid R. Foolad
2012 ◽  
Vol 55 (2) ◽  
pp. 109-123 ◽  
Author(s):  
Estelle Verzaux ◽  
Gert van Arkel ◽  
Vivianne G. A. A. Vleeshouwers ◽  
Edwin A. G. van der Vossen ◽  
Rients E. Niks ◽  
...  

2018 ◽  
Vol 17 (6) ◽  
pp. 1119-1129 ◽  
Author(s):  
Marc Ghislain ◽  
Arinaitwe Abel Byarugaba ◽  
Eric Magembe ◽  
Anne Njoroge ◽  
Cristina Rivera ◽  
...  

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 732
Author(s):  
Fergus Meade ◽  
Ronald Hutten ◽  
Silke Wagener ◽  
Vanessa Prigge ◽  
Emmet Dalton ◽  
...  

Wild potato species continue to be a rich source of genes for resistance to late blight in potato breeding. Whilst many dominant resistance genes from such sources have been characterised and used in breeding, quantitative resistance also offers potential for breeding when the loci underlying the resistance can be identified and tagged using molecular markers. In this study, F1 populations were created from crosses between blight susceptible parents and lines exhibiting strong partial resistance to late blight derived from the South American wild species Solanum microdontum and Solanum pampasense. Both populations exhibited continuous variation for resistance to late blight over multiple field-testing seasons. High density genetic maps were created using single nucleotide polymorphism (SNP) markers, enabling mapping of quantitative trait loci (QTLs) for late blight resistance that were consistently expressed over multiple years in both populations. In the population created with the S. microdontum source, QTLs for resistance consistently expressed over three years and explaining a large portion (21–47%) of the phenotypic variation were found on chromosomes 5 and 6, and a further resistance QTL on chromosome 10, apparently related to foliar development, was discovered in 2016 only. In the population created with the S. pampasense source, QTLs for resistance were found in over two years on chromosomes 11 and 12. For all loci detected consistently across years, the QTLs span known R gene clusters and so they likely represent novel late blight resistance genes. Simple genetic models following the effect of the presence or absence of SNPs associated with consistently effective loci in both populations demonstrated that marker assisted selection (MAS) strategies to introgress and pyramid these loci have potential in resistance breeding strategies.


2014 ◽  
Vol 40 (1) ◽  
pp. 10-13
Author(s):  
E. V. Rogozina ◽  
V. A. Kolobaev ◽  
E. E. Khavkin ◽  
M. A. Kuznetsova ◽  
M. P. Beketova ◽  
...  

2009 ◽  
Vol 22 (4) ◽  
pp. 437-446 ◽  
Author(s):  
James M. Bradeen ◽  
Massimo Iorizzo ◽  
Dimitre S. Mollov ◽  
John Raasch ◽  
Lara Colton Kramer ◽  
...  

Late blight of potato ranks among the costliest of crop diseases worldwide. Host resistance offers the best means for controlling late blight, but previously deployed single resistance genes have been short-lived in their effectiveness. The foliar blight resistance gene RB, previously cloned from the wild potato Solanum bulbocastanum, has proven effective in greenhouse tests of transgenic cultivated potato. In this study, we examined the effects of the RB transgene on foliar late blight resistance in transgenic cultivated potato under field production conditions. In a two-year replicated trial, the RB transgene, under the control of its endogenous promoter, provided effective disease resistance in various genetic backgrounds, including commercially prominent potato cultivars, without fungicides. RB copy numbers and transcript levels were estimated with transgene-specific assays. Disease resistance was enhanced as copy numbers and transcript levels increased. The RB gene, like many other disease resistance genes, is constitutively transcribed at low levels. Transgenic potato lines with an estimated 15 copies of the RB transgene maintain high RB transcript levels and were ranked among the most resistant of 57 lines tested. We conclude that even in these ultra–high copy number lines, innate RNA silencing mechanisms have not been fully activated. Our findings suggest resistance-gene transcript levels may have to surpass a threshold before triggering RNA silencing. Strategies for the deployment of RB are discussed in light of the current research.


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