By The Sainsbury Laboratory
By The Sainsbury Laboratory
Sept. 22, 2016, Norwich, U.K. – Plants have specialized immune receptor proteins on the surface of their cells, which detect specific molecular patterns, or ligands, on harmful bacteria.
New research by scientists at The Sainsbury Laboratory in Norwich now reveals that these immune receptors, along with the ligand that activates them, must be taken up inside the plant cell in order to mount a full immune response to bacterial infection.
When plants are attacked by harmful organisms, running away clearly isn’t an option – but that doesn’t mean they are powerless.
DETECTING AND RESISTING PESTS AND PATHOGENS
Plants have clever molecular mechanisms that help them to detect and resist pests and pathogens. Scientists at The Sainsbury Laboratory in Norwich are interested in understanding how these immune processes work because this may be useful in breeding disease-resistant crops – especially when climate change threatens to bring new pests and diseases our way.
Working with an international team of collaborators, a new study, led by The Sainsbury Laboratory’s Professor Silke Robatzek and published in the journal Proceedings of the National Academy of Science of the U.S., reveals new details about plant-triggered immunity.
Professor Robatzek explained: “We already knew that special protein molecules called ‘pattern recognition receptors,’ the immune receptors located on the surface of plant cell membranes, can recognize specific ‘microbe-associated molecular patterns,’ or MAMPs, from harmful bacteria.
An immune receptor called FLS2 is a well-studied example – this can detect flagellin, a protein found in the tube-like filaments emanating from some bacterial cells that allows them to move.
HELPING PLANT DEFEND ITSELF
Several other receptors and the associated MAMPs or danger signals that activate them have been discovered, so we know that plants can detect and resist many different types of bacteria, but we were interested in what happens next – when the receptor is activated, what does it do? Where does it go? And how, exactly, does this help the plant to defend itself?”
To answer these questions, the research team used a technique called live cell imaging in which receptor proteins of interest were tagged with a fluorescent marker so that their movements could be visualized using a special microscope.
From previous work, the scientists knew that when FLS2 is activated, it is ‘internalized.’ This means that it is moved from the plant cell membrane to a membrane-bound ‘bubble’ inside the cell called an endosome.
Postdoctoral scientist and co-first author of the study Dr. Gildas Bourdais, explains: “We discovered that several other receptors follow the same pattern as FLS2 – they too are internalized into endosomes, and they require another protein called clathrin to do so. We now show this is a common process conserved among many different immune receptors, and even danger-sensing receptors. Furthermore, we think that the process of internalisation is key to recycling the receptors so that plants stay in ‘defence mode’ in the long run.”
“BATTEN DOWN THE HATCHES”
Plants may not be able to run away, but they do have several chemical weapons at their disposal, and can also ‘batten down the hatches’ by closing their stomata – the leaf pores that usually open to allow gas exchange, but which can be infiltrated by harmful bacteria.
The scientists observed that stomata closed only when the receptor internalization mechanism was functional, strongly suggesting that it is key to providing a level of immunity even before bacteria enter the plant.
“Having lots of specialised immune receptors means that plants can sense many different MAMPs,” said Dr Bourdais said, “either from the same bacterial pathogen or different ones – but what happens next – clathrin-mediated internalization of activated receptors – is a critical step for the plant to fully deploy it’s immune responses to pathogen attack.”
This research was funded by a starting grant from the European Research Council and strategic funding from The Gatsby Charitable Foundation.