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Disease and resistance in potato

Photograph of late blight on a potato plant
Currently, multidisciplinary research at the James Hutton Institute focuses mainly on identifying and understanding resistance to the major pathogens of potato, such as late blight and potato cyst nematodes.

Cultivated potatoes are constantly exposed to various pathogens that, if successful in overcoming the plant’s defences, pose a serious threat to production. Currently, multidisciplinary research at the James Hutton Institute focuses mainly on identifying and understanding resistance to the major pathogens of potato, such as late blight, caused by the oomycete pathogen Phytophthora infestans, and potato cyst nematodes (PCN).

Since 1989 the Institute has conducted a multitrait (MT) pre-breeding programme to combine disease resistances with quality traits required for modern potato cultivars. This programme has provided parents for commercially funded breeding of finished cultivars and has delivered cultivars for various potato markets, such as Lady Balfour for organic production.

Using a combination of genetic and genomics approaches, our aim is to characterise resistance loci, develop markers suitable for marker-assisted breeding and, ultimately, to clone the genes responsible for resistance. We work in close collaboration with plant pathology colleagues. Information concerning pathogen population changes are integrated into our work, allowing us to assess the potential durability of the sources of resistance with which we work.

Late blight

Late blight, caused by the oomycete pathogen Phytophthora infestans, is the most devastating potato disease and outbreaks can have global impacts as, for example, seen during the Irish potato famine in 1845-1846 (Figure 1, below). Current management practices rely heavily on multiple fungicide applications (up to 20 per season) for disease control. Breeding for resistance is challenging as P. infestans populations are highly adaptable and have the ability to evolve quite rapidly. Indeed, a dramatic shift in P. infestans populations is currently being observed in many European potato growing regions, including the UK. New lineages of the A2 mating type appear to be more aggressive and overcome previously strong sources of resistances.

Figure 1: Late blight infected leaf

Figure 1: Late blight infected leaf.

We have previously mapped QTLs for field resistance to P. infestans from S. demissum in both diploid and tetraploid populations of potato. Efforts to clone the gene(s) responsible for strong field resistance in cv. Stirling, previously identified on linkage group IV, have shown that the gene(s) mediating resistance co-segregate genetically with resistance genes found in S. demissum (Rpi-R2), S. bulbocastanum (Rpi-blb3 and Rpi-abpt) and an additional S. demissum free cross of multiple wild species including S. tuberosum Group Andigena, S. vernei, and S. oplocense (Rpi-R2-like).

A BAC library has been generated from a resistant, dihaploid clone (HB171-13) and screened with probes derived from the above R genes. Candidate genes derived from the BAC library screen and from orthologous PCR amplification are currently functionally tested in the model species Nicotiana benthamiana.

Other genetical research focuses on resistance to late blight in the Mexican diploid species S. verrucosum. Two populations segregating for this resistance are being analysed genetically and QTL analysis is in progress.

To identify new and potentially durable forms of resistance we utilise the Commonwealth Potato Collection (CPC) by screening accessions with contemporary and diverse P. infestans isolates. A recent screen of CPC material was conducted with a complex A1 isolate, 01-29 (race 1,2,3,4,6,7,8,10,11) and BPC06_3928A (race 1,2,3,4,5,6,7,9,10,11). Strong resistance was identified in the diploid species S. bulbocastanum, S. okadae (Figure 2, below), S. polyadenium and S. verrucosum.

Figure 2: Resistant crosses of Solanum okadae

Figure 2: Resistant crosses of Solanum okadae.

Importantly, we incorporate P. infestans population and diversity data as well as pathogen ‘effector’ information to predict durability of the resistance mechanisms. The rational for including effectors is that evolutionarily conserved and non-redundant pathogen effectors may represent the pathogen’s ‘Achilles heel’. Plant resistances that recognise such effectors has the potential to be more durable than resistance towards non-conserved and non-redundant effectors. For screening, effectors are transiently expressed in resistant potato accessions using Agrobacterium tumefaciens. Typically, recognition leads to the hypersensitive response, a form of programmed cell death that is visible macroscopically.

Figure 3: Microarray results for R2 compatible (right) and incompatible (left) interaction.

Figure 3: Microarray results for R2 compatible (right) and incompatible (left) interaction.

To unravel the transcriptional changes occurring during field and R2 resistance and to identify target genes and regulatory components, a Microarray based approach utilising the Potato Oligo Chip Initiative (POCI) 44K Microarray was initiated. RNA abundance from 10 resistant and eight susceptible F1 plants from the SCRI MT168 population that segregates for field resistance and an incompatible and compatible interaction within R2 resistance background were compared respectively over a timecourse comprising basal expression at 0 h after infection (hpi), biotrophic phase at 15 hpi and at the necrotrophic phase at 72 hpi (Figure 3, above). The functional analysis of candidate genes is in progress.

You can read more information on P. infestans here.

Potato cyst nematode

The potato cyst nematodes (PCN) Globodera rostochiensis (golden potato cyst nematode) and G. pallida (white potato cyst nematode) cause over £50 million damage per annum in the UK alone. Resistance to G. rostochiensis in the form of the H1 gene has been found previously within the Commonwealth Potato Collection (CPC) and successfully introduced into the majority of potato cultivars on the UK National List. Although the H1 gene that resides on chromosome V has not yet been cloned and it’s mode of action remains elusive, the resistance has been durable for over 30 years.

However, G. pallida has become the dominant nematode threat to potato production. It has been estimated that over 60% of all potato fields in the UK are infected with G. pallida. Problems in controlling PCN are growing due to the spread of G. pallida, increase in populations, pressure to reduce nematicides and the lack of commercially attractive cultivars with resistance. Partial resistance towards G. pallida has been introduced from wild potato accession such as S. vernei and S. tuberosum Group Andigena from the CPC. Major QTLs for PCN resistance from S. vernei were found on chromosomes V and IX and for S. tuberosum Group Andigena on chromosomes IV and XI. We are currently working on development of reliable molecular markers for these QTL, the largest of which map to resistance hotspots on chromosomes IV and V.

Further information can be found on the potato cyst nematode page.


Bradshaw, J.E., Pande, B., Bryan, G.J., Hackett, C.A., McLean, K., Stewart, H.E. and Waugh, R. 2004. Interval Mapping of Quantitative Trait Loci for Resistance to Late Blight [Phytophthora infestans (Mont.) de Bary], Height and Maturity in a Tetraploid Population of Potato (Solanum tuberosum subsp. tuberosum). Genetics 168, 983-995.

Bradshaw, J.E., Hackett, C.A., Lowe, R., McLean, K., Stewart, H.E., Tierney, I., Vilaro, M.D.R. and Bryan, G.J. 2006. Detection of a quantitative trait locus for both foliage and tuber resistance to late blight [Phytophthora infestans (Mont.) de Bary] on chromosome 4 of a dihaploid potato clone (Solanum tuberosum subsp. tuberosum). Theoreetical and Applied Genetics 113, 943-951.

Bryan, G.J., McLean, K., Pande, B., Purvis, A., Hackett, C.A., Bradshaw, J.E. and Waugh, R. 2004. Genetical dissection of H3-mediated polygenic PCN resistance in a heterozygous autotetraploid potato population. Molecular Breeding 14, 105-116.

Bryan, G.J., McLean, K., Bradshaw, J.E., Phillips, M., Castelli, L., De Jong, W.S. and Waugh, R. 2002 Mapping QTL for resistance to the cyst nematode Globodera pallida derived from the wild potato species Solanum vernei. Theoretical and Applied Genetics 105, 68-77.

Hein, I., McLean, K., Chalhoub, B. and Bryan, G.J. 2007. Generation and Screening of a BAC library from a diploid potato clone to unravel durable late blight resistance on linkage group IV. International Journal of Plant Genomics, vol. 2007, Article ID 51421, 5 pages, 2007. doi:10.1155/2007/51421.


Areas of Interest

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The James Hutton Research Institute is the result of the merger in April 2011 of MLURI and SCRI. This merger formed a new powerhouse for research into food, land use, and climate change.