Plants use a multi-layered self-regulating system to control their own immune response – one that’s more intricate than anyone had previously recognized.
Understanding how it works could open up new ways to make crops more resilient without resorting to genetic modification.
The study was led by Nitzan Shabek, an associate professor of plant biology at the University of California, Davis.
In Professor Shabek’s lab, researchers work at the intersection of biochemistry and structural biology.
The hormone that cuts both ways
Salicylic acid is probably best known as the active ingredient in aspirin. In plants, it plays a completely different role – it’s a hormone that sits at the heart of the immune system, triggering defences when a pathogen shows up.
But it’s a double-edged sword: too little and the plant can’t fight off disease; too much and the plant turns on itself, developing autoimmunity and stunting its own growth.
Plants need to keep salicylic acid levels in a narrow range. What this study reveals is just how elaborate the system for doing that actually is.
A feedback loop with a twist
The basic mechanism sounds straightforward enough: when salicylic acid levels rise, the plant produces enzymes that break it down.
Two of these enzymes – known as DMR6 and DLO1 – are the main ones responsible for keeping the hormone in check.
But here’s where it gets interesting. When these enzymes bind to salicylic acid and start doing their job, their own shape changes. That change flags them for destruction by the cell’s protein-recycling machinery, a system called ubiquitin.
In other words, the very act of breaking down salicylic acid triggers a process that limits how much of it the enzymes can destroy.
The plant isn’t just turning on a cleanup crew. It’s also putting a timer on them.
“Through this layered control, plants are able to balance immunity with growth, responding quickly to threats while avoiding the cost of prolonged defense,” Shabek said.
“Our discovery could open the door for innovation in agriculture by enabling new ways to fine-tune crop immunity without compromising growth.”
Finding the regulatory protein
The story didn’t end there. By mapping how DMR6 and DLO1 interact with other proteins, the team found a previously unidentified regulatory protein they named DAF1.
It acts as the trigger that marks both enzymes for destruction – and crucially, it binds more strongly to DMR6 when salicylic acid is present.
That means salicylic acid is essentially accelerating its own inactivation, a neat piece of biological self-regulation.
“I was intrigued by the possibility that the same enzymes responsible for deactivating salicylic acid are themselves being destroyed,” said study first author Natalie Hamada, a PhD candidate in Shabek’s lab.
Testing how the protein works
To test how DAF1 actually behaves during infection, the team ran experiments on tobacco plants.
When they engineered plants to lack DAF1 entirely, the plants became more vulnerable to bacterial infection. This happened because DMR6 was free to remove salicylic acid too efficiently, leaving the immune response underpowered.
When they engineered plants to overproduce DAF1, the opposite happened: the plants showed signs of autoimmunity, their immune system running hot with nothing to rein it in.
“It’s like a seesaw – when plants don’t have DAF1, their immune response is compromised, because DMR6 removes salicylic acid too efficiently, but when they produce too much DAF1, they degrade DMR6 too efficiently, which means they end up with excess salicylic acid,” said co-author Jacob Moe-Lange.
“Regulating the regulators of salicylic acid is critical for plants to successfully grow and balance priorities when they face stress.”
What this means for agriculture
There’s a practical dimension to all this. Researchers have known for a while that engineering plants to reduce DMR6 activity can boost immunity.
The problem is that it also tends to hurt plant growth and it comes with the regulatory complications that accompany any genetically modified crop.
DAF1 offers a potentially more precise lever. Rather than permanently altering the plant’s genetics, it might be possible to develop molecules that tweak the interaction between DMR6 and DAF1.
This could ultimately give scientists the ability to nudge the immune system up or down as needed, without permanently changing the plant’s DNA.
“Our findings could potentially be used to fine-tune plant disease resilience without using genetic engineering,” Hamada said.
“For example, it might be possible to design molecules that enhance or inhibit interactions between DMR6 and DAF1, which could be strategically applied to non-GMO crops.”
That’s still a few steps away. But the discovery of DAF1 gives plant scientists a new target to work with – and a clearer picture of a system that, it turns out, is considerably more sophisticated than it looked.
The study was published in the journal Nature Communications.
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