This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
I have a soft-spot for plant biology. In my final year at university, having exhausted all of the bacteria-related biochemistry lectures, I took a bacteria-related lecture course with the plants department. It was a smaller department, and seemed a lot friendlier and nicer. Also the biscuits in the tea-room were cheaper.
So I do like to write about plants every now and again, and it isn't a very difficult task because like every other multicellular organism on the planet, plants also suffer from bacterial infections. Unlike humans, they don't have a blood stream to carry immune cells around, so they instead rely on bombarding bacteria with nasty chemicals, quickly killing off any parts of the plant that get infected and acquiring a kind of plant resistance to stop attacks occurring again. (The three links are to a mini-series on plant immunology on my old blog.)
However in plants, as in humans, prevention is much better than cure and so the plant has all sorts of mechanisms to stop bacteria getting inside and causing infections in the first place. Plants have openings in their leaves called stomata which are used to control water levels inside the plant cells. The stomata open up to release moisture and close to retain it. They aren't massive holes, but they can be seen with a light microscope and identified fairly easily by your average 16 year old (I remember looking at them during my AS levels!)
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As stomata are basically a hole from the inside of the plant to the great bacteria-ridden outdoors, it is important that they remain well-regulated. Plants can recognise bits of bacteria and when they do they can change internal conditions to close up the stomata, bolting the doors to prevent bacteria getting in. By sensing parts of bacteria such as (say) flagella, proteins are activated that change the concentrations of salts inside the cells surrounding the stomata, and cause them loose their curved shape and come together, effectively closing off the opening.
When plants were infected with the bacterial strain of Pseudomonas syringae the stomata closed up within 1-2 hours of infection, which for a plant is fairly rapid. However around 3-4 hours later the stomata started opening up again, and it wasn't due to a bacterial protein, but a plant one. The protein in question was LecRK-V.5 and plants without the gene for this protein developed fewer disease symptoms and contained lower levels of internal bacteria than the non-mutated wild-types. The figure below shows the wild-type leaves at the top, with more disease symptoms than the healthier mutants below.
As stomatal opening is only one factor in the antibacterial plant response, the researchers then explored whether LecRK-V.5 was affecting any other responses. The main one being the production of dangerous Reactive Oxygen Species (ROS) which are often produced to damage invading bacteria. Both wild-type and LecRK-knockout-mutant plants showed no difference in levels of ROS, LecRK-V.5 only seems to affect the stomata.
The point about ROS also gives a clue as to just why the plant chooses to activate this protein following infection, seemingly making it easier for bacteria to gain access to the interior. In the mutant plant cells, with no LecRK-V.5, high levels of ROS started building up in the cells surrounding the stomata. ROS are dangerous to any cell they come into contact with, so by dampening down the response to bacterial infection around 4 hours following entry, the plant might be saving itself from being damaged by its own immune response. If the infection is still spreading after four hours, it may be more prudent for the plant to abandon the dead tissue and try and salvage what's left. Leaves are not desperately important to plants after all, they can always grow more!
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Ref 1:Desclos-Theveniau, M., Arnaud, D., Huang, T., Lin, G., Chen, W., Lin, Y., & Zimmerli, L. (2012). The Arabidopsis Lectin Receptor Kinase LecRK-V.5 Represses Stomatal Immunity Induced by Pseudomonas syringae pv. tomato DC3000 PLoS Pathogens, 8 (2) DOI: 10.1371/journal.ppat.1002513
Ref 2: Nicaise, V., Roux, M., & Zipfel, C. (2009). Recent Advances in PAMP-Triggered Immunity against Bacteria: Pattern Recognition Receptors Watch over and Raise the Alarm PLANT PHYSIOLOGY, 150 (4), 1638-1647 DOI: 10.1104/pp.109.139709
Credit for image 1.
