Robigalia Roundup LXXIX: An internal alarm system nobody knew existed

Hello {{first_name | Robigalia readers}},

I'll apologise in advance to all the non-molecular folks in this community, but something came out this week that was too exciting for me to leave out of the opening notes.

A paper published in Science on 30 April has just upended one of the foundational assumptions in plant immunity. For those not deep in the molecular world, here's the short version: for years, scientists believed that when a plant detects a pathogen, its immune receptors do their work at the outer boundary of the cell, the plasma membrane. That's where they were thought to form pore-like structures and let calcium flood in as a rapid distress signal, triggering defence. This was the accepted model.

What researchers at Imperial College London, The Sainsbury Laboratory, Academia Sinica, and the Bezos Centre for Sustainable Protein have now shown is that a class of immune receptors called NRG1, part of the NLR (nucleotide-binding leucine-rich repeat) family that many of you will know well, doesn't only work at the plasma membrane.

NRG1 can target the membranes of organelles inside the cell, particularly chloroplasts, and release calcium stored within them instead. Essentially, plants have an internal alarm system that nobody knew was there.

What makes this story even better is how it was found. Early experiments showing NRG1 accumulating in chloroplasts were so unexpected that they were initially set aside.

Then AlphaFold 3 entered the picture and consistently predicted a funnel-shaped NRG1 structure that could span a double membrane, the exact architecture of an organelle. Suddenly a strange result had a mechanistic explanation, and the team went back to dig deeper.

The implications for durable resistance breeding are worth watching closely.

Before I hand you over to this week's edition, I want to ask you something.

Currently, research papers feature as part of the Pathogen of the Week write-up. But I'm wondering whether you'd find value in a dedicated section highlighting noteworthy papers from the previous week across plant pathology more broadly, not just those tied to the featured pathogen.

Now, onto this week’s edition:

Let’s dive in!

When wheat farmers across the American Midwest began losing billions of dollars' worth of grain to a disease called "scab" in the 1990s, they were witnessing the re-emergence of a pathogen that had terrorised cereal crops for over a century. Fusarium head blight (FHB) was first described in 1884 in England and was considered a major threat to wheat and barley during the early years of the twentieth century. From 1993 to 2014, wheat farmers in the United States lost $17 billion worth of wheat due to FHB. Few plant diseases combine such devastating yield losses with the insidious threat of toxic contamination.

Fusarium graminearum (sexual stage: Gibberella zeae) is an ascomycetous fungus belonging to the Nectriaceae family within the order Hypocreales. This pathogen has evolved a remarkable dual strategy for survival and destruction. It functions both as a saprophyte, thriving on crop residues in soil, and as an aggressive parasite that colonises living plant tissues. The fungus produces two types of spores, asexual macroconidia that spread locally during the growing season, and sexual ascospores that can disperse over vast distances, enabling long-range colonisation and genetic recombination that drives pathogen evolution.

Fusarium graminearum attacks wheat, barley, oats, maize, and numerous grass species, causing the disease known as Fusarium head blight or scab. Infected wheat spikelets are bleached, appearing water-soaked initially before turning chalky white, often progressing sequentially through the head as salmon-orange spores of F. graminearum become visible on glumes. Infected wheat and durum kernels are sometimes called "tombstones" because of their shrivelled, chalky, lifeless appearance that may also look pink. Beyond the visible damage, the fungus produces potent mycotoxins, particularly deoxynivalenol (DON, also called vomitoxin) and zearalenone, which contaminate grain and pose serious risks to human and animal health.

The pathogen has achieved near-global distribution across temperate cereal-growing regions. FHB is currently the most economically important wheat disease in the U.S. and Canada, whilst in China more than 9.9 million hectares were affected in the main producing areas in 2012. In Latin America, seventeen epidemics have been reported in Argentina from 1960 to 2012 with losses of up to 70% in some years. The disease flourishes under warm, humid conditions, particularly during flowering when prolonged periods (48 to 72 hours) of high humidity and warm temperatures create perfect infection conditions.

Management requires an integrated approach combining host resistance, cultural practices, and strategic fungicide applications. Host resistance is important but mostly has been found in bread wheat, and less resistance has been found in durum wheat yet, although major resistance genes found in bread wheat, such as Fhb1 and Fhb7, were successfully integrated into durum wheat.

Crop rotation away from cereals and maize, along with tillage to bury infected residues, reduces inoculum build-up. Chemical control through fungicides plays a significant role, although the continuous exposure causes a selection pressure in the pathogen population towards fungicide resistance. Triazole fungicides remain the primary chemical control tool, but timing applications at early flowering is critical for effectiveness.

The search for new tools to combat this pathogen continues to drive research. Modern approaches increasingly combine metabolomics with genome editing technologies to understand how plants can be engineered for enhanced disease resistance, particularly in durum wheat varieties that have historically shown high susceptibility to FHB.

Keep reading to meet a plant pathologist whose doctoral research applies exactly these cutting-edge techniques to tackle F. graminearum.

This week, we meet Krishna Kumar, a plant pathologist who recently completed his doctorate at McGill University in Canada and has since moved into a laboratory analyst role at Pathogenia Lab in Montreal, bringing his expertise in metabolomics and genome editing to an applied diagnostics setting.

Krishna's path into plant pathology began in India, where his biotechnology training first exposed him to the scale of crop losses caused by plant pathogens. Watching diseases undermine productivity and food security in a country where wheat, lentils, and chickpeas are agricultural staples gave his research a clear purpose from the start.

His early career took him through several of India's leading agricultural research institutions. Beginning as a Project Assistant at ICAR-National Bureau of Plant Genetic Resources, he progressed to Senior Research Fellow on an ICAR-ICARDA collaborative project focused on breaking yield barriers in lentil and chickpea, where he led interspecific hybridisation work and hybridity confirmation using DNA fingerprinting.

He later held Junior Research Fellow positions at the Indian Agricultural Research Institute, working on white rust-resistant mustard, and at BRIC-National Institute of Plant Genome Research, where he developed transgenic chickpea lines. By the time he arrived at McGill, he had accumulated over a decade of hands-on experience across tissue culture, marker-assisted selection, and plant transformation.

His doctoral research centred on Fusarium graminearum, the fungal pathogen responsible for Fusarium Head Blight (FHB), a disease that threatens global wheat production by slashing yields and contaminating grain with mycotoxins. Durum wheat, the foundation of pasta production, is particularly susceptible, making resistance a pressing goal for breeders and food safety researchers alike.

Krishna approached the problem from two directions: using LC-MS/MS metabolomics to identify resistance-associated secondary metabolites in F. graminearum-inoculated resistant and susceptible varieties, and developing a multiplex CRISPR/Cas9 genome editing pipeline targeting the susceptibility gene TdHRC in durum wheat. The work establishes a functional genomic tool for durum improvement and was recognised through the McGill Graduate Excellence Award and the Young Scientist Award.

Alongside his research, Krishna has qualified as a Certified Canadian Patent Administrator and has been active in patent preparation and prosecution since 2024, reflecting a sustained interest in how scientific innovation moves from the laboratory into practice.

You can connect with Krishna on LinkedIn to follow his work as he transitions from doctoral research into the next phase of his career.

Have a job, scholarship, or event to advertise? List it in Robigalia. I’ll help promote your opportunity or event to a global network of over 10,000 plant pathologists for free.

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: