Viviana Sosa-Zuniga, Álvaro Vidal Valenzuela, Paola Barba, Carmen Espinoza Cancino, Jesus L Romero-Romero, Patricio Arce-Johnson
9 min
Grapevine (Vitis vinifera) cultivation is a massive global industry, yet it faces persistent pressure from the biotrophic fungus Erysiphe necator, the causal agent of powdery mildew. This pathogen significantly reduces crop yields and compromises fruit quality—affecting sugar content, acidity, and sensory characteristics of the final wine. Currently, managing this disease relies heavily on intensive fungicide applications, which are costly, pose health risks to workers, and have negative environmental consequences. As consumers and regulators increasingly demand more sustainable agricultural practices, genetic improvement of grapevines has emerged as a critical focus area.
The Vitaceae family, which includes grapevines, possesses natural genetic resistance to powdery mildew, primarily mediated by two gene families: Run (Resistance to Uncinula necator) and Ren (Resistance to Erysiphe necator). These genes generally encode NBS-LRR (nucleotide-binding site leucine-rich repeat) proteins, which act as molecular sensors within the plant. When these proteins recognize pathogen effectors, they trigger an immune response known as effector-triggered immunity (ETI). Common host responses include the rapid accumulation of reactive oxygen species (ROS), the deposition of callose at infection sites, and programmed cell death (PCD) to prevent the fungus from obtaining nutrients and spreading.
A major challenge in breeding resistant cultivars is the pathogen's tendency to evolve and overcome individual resistance genes. To address this, breeders are utilizing a strategy known as gene pyramiding, which involves stacking multiple resistance loci into a single genotype. Research indicates that combining specific loci—such as Run1 and Ren1—can lead to stronger, additive immune responses compared to individual gene action. However, this is not a universal rule; some combinations do not result in enhanced resistance. Selecting the optimal combination of loci from diverse geographic origins is essential for developing varieties that can maintain resistance over their long 20-year productive lifespans.
While traditional cross-breeding remains a cornerstone of viticulture improvement, it is time-consuming. Emerging techniques like CRISPR-Cas9 genome editing are being explored to knock out susceptibility (S) genes to enhance natural resistance. A vital area for future research is assessing the physiological costs of these resistance traits; it remains to be seen if the energy redirected toward immune defense significantly impacts photosynthetic rates or vine health.
Grapevine (Vitis vinifera) is one of the main fruit crops worldwide. In 2020, the total surface area planted with vines was estimated at 7.3 million hectares. Diverse pathogens affect grapevine yield, fruit, and wine quality of which powdery mildew is the most important disease prior to harvest. Its causal agent is the biotrophic fungus Erysiphe necator, which generates a decrease in cluster weight, delays fruit ripening, and reduces photosynthetic and transpiration rates. In addition, powdery mildew induces metabolic reprogramming in its host, affecting primary metabolism. Most commercial grapevine cultivars are highly susceptible to powdery mildew; consequently, large quantities of fungicide are applied during the productive season. However, pesticides are associated with health problems, negative environmental impacts, and high costs for farmers. In paralleled, consumers are demanding more sustainable practices during food production. Therefore, new grapevine cultivars with genetic resistance to powdery mildew are needed for sustainable viticulture, while maintaining yield, fruit, and wine quality. Two main gene families confer resistance to powdery mildew in the Vitaceae, Run (Resistance to Uncinula necator) and Ren (Resistance to Erysiphe necator). This article reviews the powdery mildew resistance genes and loci and their use in grapevine breeding programs.
Sam: That makes recognition a potential weak point. If the fungus changes what the plant recognizes, the defense could fail.
Alex: That's the risk the authors describe. One response to recognition is programmed cell death, where infected cells die and restrict fungal development. Other responses include reactive oxygen production and deposits of callose, a material that can form a barrier. Different resistance sources trigger these responses at different stages and strengths.
Sam: When the authors name those sources, are they talking about identified genes, or just regions associated with resistance?
Alex: Mostly regions. A locus is a region of a chromosome, not necessarily a single identified gene. The review groups these resistance regions under the names Run and Ren. For most, the causal genes and detailed mechanisms remain unclear.
Sam: Is there a case where researchers moved beyond that association and tested a particular gene?
Alex: Run1 is the clearest example. Researchers narrowed its location, identified candidate genes, and introduced full-length candidates into susceptible grapevine varieties. They then measured the death response in cells penetrated by the fungus. That work identified the resistance gene called MrRUN1.
Sam: Identifying a working gene sounds useful, but does that protection hold against every fungal strain?
Alex: No. The review describes isolates that overcame Run1 resistance, while protection remained against the most widespread genetic groups in viticultural areas. The resistance-breaking isolates were reported only in southeastern North America. So the review argues that both the resistance source and the local pathogen population matter.
Sam: Then combining sources sounds sensible, especially from different geographic origins. But your opening warned that combinations don't necessarily improve protection.
Alex: Here's the distinction. Pyramiding means combining multiple resistance regions in the same plant. The proposed goal is durable protection through defenses with different mechanisms and different strain coverage. A stronger immediate response would be useful, but it isn't the same as demonstrating long-term durability.
Sam: Can we put a number on that immediate response, rather than just calling one source strong and another weak?
Alex: Consider Ren6 and Ren7, found in a Chinese grapevine species. In Ren6 plants, roughly ninety-two to ninety-five percent of infected cells showed an effective programmed death response. In Ren7 plants, the corresponding proportion was about ten to twenty percent. Ren6 also acted earlier, limiting fungal development more effectively.
Sam: Those are percentages of infected cells, not percentages of vines protected or harvest saved. What happened when researchers combined the sources?
Alex: Plants carrying both showed no difference in disease development compared with plants carrying Ren6 alone. In that comparison, adding the weaker source didn't improve the measured response. The review gives other examples where stacking also produced no additive effect.
Sam: Is there a positive counterexample, or does the evidence mostly challenge the stacking strategy?
Alex: There are positive examples. Combining Run1 with Ren1 produced stronger responses than either source alone. Researchers observed more reactive oxygen production, more callose accumulation, and more programmed cell death. They also reported greater activation of defense-related genes.
Sam: So the useful result is selective: some combinations improve measured defenses, and others don't. How far does that take us toward a vineyard recommendation?
Alex: Not all the way. These are comparisons assembled from separate studies, not a pooled field estimate. The highlighted cellular results don't come with sample sizes in this excerpt. And grapevines remain productive for at least twenty years; these comparisons don't establish protection across that lifespan.
Sam: The review also discusses editing. Does that mean inserting resistance genes, or changing something the fungus needs from its host?
Alex: The section focuses on susceptibility genes: plant genes whose inactivation can increase resistance. In grapevine, silencing several members of the mildew locus O gene family reduced infection by seventy-seven percent. That's a separate reported experiment, not a measured benefit of the resistance combinations we've discussed.
Sam: Removing susceptibility sounds attractive, but those genes may have other jobs. Does the review identify that trade-off?
Alex: Yes. Editing another member of that family increased resistance in plants carrying one mutated copy. Plants with both copies mutated died from tissue necrosis. That suggests the gene has additional functions, and shows why increased resistance alone isn't enough to establish a useful breeding outcome.
Sam: We've covered strain coverage and durability. What's the biggest unresolved issue for judging whether resistant vines remain productive?
Alex: The physiological cost of resistance. The authors say it hasn't been established whether these resistance sources alter photosynthesis or carbon assimilation. Alongside the uncertain mechanisms, that's a major gap: we need to know not just whether the fungus is stopped, but how the resistant plant performs.
Sam: Who should read the full review, and where should they begin?
Alex: Grapevine breeders and researchers studying plant immunity should start with “Locus Stacking: The Search for Durable and Broad-Spectrum Resistance.” Then read the individual resistance-source sections relevant to their material. The final remarks identify the missing physiological evidence. For everyone else, remember this: more resistance sources do not automatically mean better or lasting protection.
Sam: Thanks for listening.