Late Blight - Is Resistance Futile? 2

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This was an article I wrote for the Badger Common’Tater, the trade journal for the Wisconsin Potato and Vegetable Growers.

Friday, July 1, 2011









Every potato and tomato grower has probably lost sleep at some point worrying about the possibility of a late blight epidemic in their state, their county, or (in the worst case scenario) their own fields.  The worries stem from the fact that, unless they are one of the few people growing resistant cultivars, the crop they have in the field looks like an all-you-can-eat buffet to a few hungry late blight spores. 


In places like Central and South America, wild potato populations exist as a mixed collection of plants that aren't all genetically identical to one another.  This allows the population to adapt and survive even under intense pressure from pathogens such as late blight.  Some (or most) individuals in wild populations are susceptible and, when the disease spreads, will die without passing on their genetic information to the next generation.  However, the resistant individuals will flourish and pass on the valuable trait to their progeny. Therefore, the species as a whole will survive.  Growing potato in an agricultural setting is quite different, however.  A field of potatoes contains plants that are all genetically identical to one another, and they will all react in the same way to the environment, including exposure to late blight.


Unfortunately, the vast majority of potato varieties are late blight susceptible.  This is likely due to a breeding "bottleneck" when potato was first introduced to Europe in the second half of the 16th century.  The lack of genetic diversity among potatoes became apparent in the mid-1800's during the Great Irish Famine.  Since then, breeders have been actively pursuing the development of late blight resistant varieties.


Wild potato species have provided natural rich resistance sources against late blight.  Solanum demissum is a Mexican species from which 11 genes for resistance have been identified and used in potato breeding.  In the 1930's there was great optimism that the incorporation of these genes would completely eliminate late blight in North America.  Unfortunately, their optimism was misplaced.  Because of the popularity of the new cultivars, there was an intense selective pressure on late blight to evolve and overcome resistance. New strains of late blight rapidly overcame the resistance genes from S. demissum in most potato growing regions.  Even the combination of multiple genes, called "pyramiding", into a single cultivar proved ineffective.  The cultivar ‘Pentland Dell’, which contained three different genes for resistance was released for production in 1963.  By 1967, new late blight strains arose that could overcome the resistance.  Despite this, breeders have continued to incorporate novel sources of late blight resistance.  Some recent US cultivars include ‘Defender’ (Rich Novy, ID), ‘Missaukee’ and ‘Jacquelline Lee’ (David Douches, MI).  The genes involved in resistance in these cultivars are currently unknown, so we will have to wait and see how well they withstand late blight’s rapid evolution.


A great deal of work has also been done using resistance from the wild species S. bulbocastanum. This species contains three different resistance genes - RB (also called Rpi-blb1), Rpi-blb2, and Rpi-blb3.  All three are very effective at providing resistance to many different strains of late blight.  However, since S. bulbocastanum cannot be crossed with cultivated potato, their integration and deployment has been impeded.  Somatic fusions (non-sexual recombination of two plant cells) can be used, but this process brings with it a lot of "wild" potato traits that are difficult to remove.  Somatic fusions between S. bulbocastanum and cultivated potato were made in the mid-1990's by Dr. John Helgeson (USDA/ARS, UW-Plant Pathology).  In collaboration with Dr. Shelley Jansky (USDA/ARS, UW Horticulture), the Halterman Lab is continuing to work with the somatic fusion derivatives to integrate other valuable traits, such as early blight resistance, in order to develop useful germplasm for breeders.  In the mean time, late blight continues to evolve and there is no guarantee that new cultivars released years from now will continue to be resistant.  A speedier process is to integrate resistance using genetic modification, which allows introduction of a single gene - or pyramiding of multiple genes in the same amount of time.  This process is not only fast (it takes about 6 months), but avoids the introduction of undesirable traits from wild potato.  The result is a potato or tomato that grows and produces just like the original, but is now resistant to late blight.  The only hurdle at this point is public acceptance of crops that have been genetically improved in this way.  This method also does nothing to stop late blight from overcoming resistance within a few years. 


Why is late blight able to overcome resistance so quickly?  The answer lies within the genome of Phytophthora infestans, which contains all the information needed for this pathogen to grow and reproduce.  The entire genome of P. infestans has now been sequenced, revealing all the factors that are potentially involved in causing disease.  In order to cause disease, all plant pathogens (bacteria, fungi, nematodes, etc.) produce molecules that enter plant cells and make modifications to create a better living environment.  It's kind of like someone breaking into your house, turning off the alarm system, resetting the thermostat, doing laundry, making dinner, watching TV, and eating all your food - all on your bill! These pathogen molecules are called "effectors" because their presence results in some effect on the plant.  It is estimated that there are about 500-600 effectors secreted by P. infestans in order to modify potato or tomato to make it a better living environment (imagine 600 people breaking into your house).  Compared to other pathogens, this is an enormous number of effectors and is most likely the reason why late blight has proven so adaptable.


The Halterman lab has recently been most interested in late blight effectors that directly affect the activity of plant resistance genes - specifically the RB gene.  RB acts as a sentry within the plant and, when it recognizes the presence of a pathogen effector, it flips a molecular switch that turns on the plant's defense system.  What is somewhat troubling (but not unexpected), is that some P. infestans strains contain an effector that functions to sabotage RB and render it useless.  We have been very successful in understanding the mechanism that P. infestans uses to accomplish this.  Our work is now focused on identifying RB-like genes from wild species of potato or engineering new RB variants that are invulnerable to the activity of P. infestans effectors in order to try to stay one step ahead of late blight.


In the end, resistance to late blight is probably not futile, but it can sometimes feel like it.  When you consider that it takes 10-15 years to develop a potato cultivar and that late blight can overcome resistance in 5 years or less, the math doesn't seem to add up.  However, advanced technologies are now available to speed up the breeding process, and our ongoing efforts to understand how late blight causes disease will make us prepared to identify and deploy resistance quickly and effectively.