Robigalia Roundup LXXXIV: The plant receptor that fools a pathogen into attacking the wrong target

Hello {{first_name | Robigalia readers}},

This week, I want to ask you something.

I've been pondering over it for a while now and a recent run of editions has brought it back into focus for me.

Over the past few editions, I've covered papers that touched on plant pests alongside pathogens, and the response has been positive. It made me think more carefully about the boundaries of what this newsletter covers as I recognise plant pathology doesn't exist in isolation.

Pests, pathogens, biosecurity, and surveillance are tightly connected. I know many of my readers work across those boundaries, and I want to know whether you'd like Robigalia to reflect it too.

I'm not announcing any changes right now, but if there are in the future, I want those changes to be driven by you as the readers and pathologists.

My question to you as my readers, is if you would like to see Robigalia expanded to cover more topics in plant health and biosecurity, rather that just plant pathology?

You can let me know in the poll below 👇

My inbox is always open for longer responses, or even a chat. A direct reply to this email reaches me.

Replies may be a little slow at the moment, but I promise to get back to all of you!

Now, onto this week’s edition:

Let’s dive in!

This week's paper is one of the most technically intricate I've covered in Robigalia, and given the breadth of this readership, I'll do my best to communicate what is a remarkable set of findings while trying not to lose anyone in the molecular detail.

When a plant pathogen invades, it injects effector proteins that target and manipulate host molecules. One counterstrategy plants have evolved is to produce immune receptors that mimic those targeted host molecules, so that the effector binds the receptor instead and triggers immunity.

A paper by Gómez De La Cruz et al., published last week in Science, reports that a barley immune receptor has evolved to detect a pathogen effector by mimicking the effector's host target. MLA3 recognises the Magnaporthe oryzae effector Pwl2, which normally targets a host protein called HIPP43.

The authors show that MLA3 has evolved to mimic HIPP43's binding interface, so that Pwl2 binds MLA3 instead of HIPP43 and triggers an immune response. The two proteins share no sequence similarity and differ substantially in overall structure, but at the interface where Pwl2 makes contact, they present an equivalent binding surface.

The evidence is extensive. AlphaFold2 structural modelling, binding assays, and cell death experiments in Nicotiana benthamiana all confirmed the mimicry. The authors traced recognition to three amino acids unique to MLA3. A single amino acid substitution in MLA23, the most closely related allele that does not recognise Pwl2, was sufficient to confer recognition. The reverse substitution in MLA3 abolished it.

Armed with this understanding, the authors engineered a receptor that recognised both effectors. They grafted MLA3's Pwl2-binding interface onto SR50, an immune receptor from rye that confers resistance to wheat stem rust (Puccinia graminis f. sp. tritici). The chimeric SR50 retained its original stem rust resistance and gained resistance to blast. Transgenic barley lines expressing this receptor were resistant to both pathogens.

The result raises a broader possibility. Resistance receptors may be modular enough to combine recognition specificities, potentially offering a path toward single-gene solutions to multi-pathogen disease problems.

The story of Plasmopara viticola and the Bordeaux mixture is one of plant pathology's more charming origin stories. In 1882, botanist Pierre-Marie-Alexis Millardet noticed that the grapevines along a Bordeaux roadside, treated with a copper sulfate and lime mixture to deter thieves, showed no symptoms of downy mildew while the rest of the vineyard was infected. That accidental observation led to the publication of Bordeaux mixture in 1885, giving growers their first effective tool against a pathogen that had arrived from North America with the phylloxera rootstocks and devastated European viticulture within the decade. Copper has remained central to downy mildew control ever since, which gives you some sense of how difficult this pathogen is to replace.

Plasmopara viticola (Berk. & M.A. Curtis; Berl. & De Toni) is an obligate biotrophic oomycete in the order Peronosporales, incapable of completing its life cycle without a living host. Native to eastern North America, it was introduced into Europe in the 1870s, possibly with wild American Vitis species imported as phylloxera-resistant rootstocks, and after its first description in France in 1878 rapidly reached southern and central Europe before spreading to virtually every wine-producing country worldwide.

The pathogen overwinters as thick-walled oospores capable of surviving adverse conditions for years. These germinate in spring when temperatures exceed 10°C and rainfall triggers the release of biflagellate zoospores, which are then dispersed by rain splash onto host tissue.

Plasmopara viticola attacks all green tissues of Vitis vinifera and related species, with leaves, shoots, and developing berries all susceptible. The disease is characterised by oily patches on the upper leaf surface that develop a dull green to yellow colour, while the underside exhibits white sporangiophore growth visible as a downy coating under humid conditions. Infection causes leaf discolouration, necrosis, and defoliation, collectively reducing sugar accumulation in berries and overwintering capacity of buds. Young infected berries turn brown and become covered in white sporangiophore growth. As berries ripen they become less susceptible, though rachis infections can spread into older fruit.

The pathogen is now present across all major grapevine-growing regions. Infected grapevines may suffer crop yield reductions of up to 80% under high disease pressure, and in France, vineyards covering just 3.3% of agricultural land accounted for 14.4% of national fungicide use in 2006. Wide application of single-site fungicides throughout the twentieth century has driven the emergence of resistant strains across multiple fungicide classes, complicating control programs significantly.

Management relies on combinations of copper-based products and systemic fungicides applied according to weather-based warning systems, with fungus-resistant cultivars increasingly entering commercial production. These cultivars carry introgressed resistance loci from wild Vitis species and can reduce fungicide applications per season from nine or more to as few as two or four. Susceptible varieties still dominate commercial production and cannot practically be grown without chemical intervention, which is driving interest in lower-toxicity biochemical alternatives.

Enzymes and biosurfactants are among the approaches now being investigated. That's the focus of this week's Plant Pathologist of the Week.

This week, we meet Alejandra Valencia, a plant pathologist from Colombia, currently in the first year of her Master's in Phytopathology at the Federal University of Lavras in Brazil.

Alejandra arrived at agronomy through a lifelong need to understand how things work. She spent much of her childhood as a clarinettist, but the pull toward science proved stronger. Phytopathology found her early in her undergraduate studies at the Politécnico Colombiano 'Jaime Isaza Cadavid', before she had the vocabulary to distinguish one disease from another. A professor in those first semesters left a lasting impression, not through the complexity of what he taught, but through his ability to make complex ideas legible through simple, concrete examples. That approach shaped how Alejandra thinks about science communication to this day.

Her undergraduate years at the Politécnico were research-dense. Greenhouse trials evaluated the biocontrol potential of Bacillus spp. against the root-knot nematode Meloidogyne incognita in tomato and lettuce. Separate bioassay work assessed the antifungal activity of essential oils and extracts from Piper sp. against Fusarium oxysporum f. sp. cubense Race 1. She also served as a teaching assistant in phytopathology on multiple occasions, and before leaving for Brazil, completed a contract role in the molecular identification of fungal and bacterial isolates of agricultural interest. That range of experience, across biocontrol, chemical ecology, diagnostics, and teaching, gave her a broad foundation before she narrowed her focus for postgraduate work.

Now in her Master's at UFLA, she works with the oomycete Plasmopara viticola, the causal agent of grapevine downy mildew. Her research focuses on biochemical alternatives for integrated disease management, specifically enzymes and biosurfactants, with the aim of reducing reliance on synthetic fungicides through low-toxicity, environmentally sustainable options. She is the first person in her family to pursue postgraduate study, and to do so in another country.

You can connect with Alejandra on LinkedIn or follow her on Instagram at @alevalr03.

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See you next Monday!

P.S. Why Robigalia? The name originates from the Ancient Roman festival dedicated to crop protection. You can read all about the history here: