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Late blight keeps farmers, breeders, and scientists on their toes. Despite 180 years of research since Montagne identified the culprit in 1845, the battle between the oomycete Phytophthora infestans and science continues. But the tool kit of science is getting full of novel instruments. Recently, scientists from McGill University and the International Potato Center wrote an excellent, comprehensive review on the genetic basis of late blight resistance. They demonstrated that new insights into the genetic base of resistance and immunity offer novel approaches in breeding and disease management. Time to take stock.
The causal agent of late blight is a nasty oomycete. The genome of P. infestans is extremely dynamic, because of the many transposons and repeats. Populations of P. infestans are versatile and aggressive, can break “new” resistance genes rapidly, and become rapidly resistant against fungicides. There are promising new breeding tools, such as diploid hybrid breeding, allowing more rapid stacking of resistance genes. However, the entire potato sector needs to be frugal with the available resistance genes: resistance requires management through a community approach that guarantees prolonged success. Even resistance based on stacked resistance genes (Rpi genes) can be broken disappointingly fast. Keeping track of the emergence of resistance-breaking P. infestans isolates is essential for effective deployment of Rpi genes. Moreover, resistant cultivars need to be sprayed with fungicides wisely during cultivation to keep the resistance intact. Organic potato growers have a special responsibility to kill the vines of their crops timely.
Seventy resistance genes have been identified and localized in 32 Solanum species. Yet, only about twelve of them are being actively used in potato breeding programmes. Introgressing these resistance genes into cultivars is not simple. Complicating factors include tetrasomic inheritance, linkage drag, differing endosperm balance numbers, the requirement of many backcross generations, complicated phenotyping in the field, etcetera. Possible solutions for this complexity are diploid hybrid breeding, somatic hybridization, and genetic engineering through cisgenesis or CRISPR-Cas approaches. But also with these solutions, resistance management is crucial to avoid rapid resistance breakdown by the versatile oomycete. Stacking or pyramiding resistance genes is an excellent strategy to make the resistance longer lasting. Pyramiding will slow down resistance breakdown. Yet, also in cultivars with two or even three stacked Rpi genes, resistance can break down surprisingly rapidly when they are grown under strong disease pressure.
A completely different approach would be to genetically engineer S (susceptibility) genes. These S genes facilitate late-blight development by supporting initial infection or oomycete growth after infection or suppressing immune responses. Changes in these S genes might make it more challenging for the pathogen to establish a successful infection thus impairing its impact.
In addition to Rpi and S genes, plant immunity offers new opportunities to combat late blight. For example, PERU is a pattern recognition receptor at the plant cell surface. It recognizes an immunogenic peptide derived from a cell wall glycoprotein that is produced by all P. infestans isolates. Binding of this peptide to PERU triggers an immune signalling cascade in the potato plant leading to a hypersensitivity response and other immunity-related responses. Expression of the PERU gene in a susceptible potato confers enhanced resistance to late blight. Phylogenomics studies suggest that the PERU receptor family has originated in the Andes and is not present in more northern lineages of wild Solanum species.
Chloroplasts in epidermal tissue can also play a significant role in immunity of a plant host. They can serve as the first line of defence against a broad spectrum of pathogens, including P. infestans. They do so through their so-called epidermal chloroplast response: a physical movement of chloroplasts and associated immune components, specifically in epidermal cells. This concentrates all kinds of defence mechanisms to the site of the pathogen attack, maximizing the overall efficiency of the defence. Such mechanisms can support avenues towards durable resistance. But a lot of research is required to fully unravel the genetic bases of these mechanisms.

We cannot afford to solely rely on single-gene resistance or solely on application of fungicides. We need to combine gene stacking, introgression of new immunity genes, resistance management, including monitoring the pathogen population, and spraying resistant cultivars with alternating fungicides to control late blight. We can do so with minimal harm to the environment, minimal yield losses and minimal cost to growers and society. ●
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