how a fungus avoids a plant’s immune system

Your immune system is a wonderful, complex, multipartite mechanism that usually allows you to fight off the attentions of the various pathogenic organisms (bacterial, fungal, and viral) that you’ll meet during your life. I say ‘usually’ because it’s not always successful on its own, and even where it is, you can be laid low for quite some time – think of flu, but also think of measles, mumps, smallpox, polio… This is where vaccination comes in: this ‘primes’ your immune system so that it can react far more rapidly when it encounters the actual pathogens themselves. NB for a taste of some ‘alternative’ thinking on this concept, try this thread over on SciBlogsNZ.

Now, all multicellular animals have some form of immune system. Ours offers two modes of defence: an ‘innate’ immune system, plus the ‘adaptive’ system involving antibody production in response to the multitude of antigens we face each day. At the other end of the scale, things like jellyfish & sea anemones have only the innate component. For example, Hydra (a freshwater version of the more familiar sea anemones, greenish in colour due to the presence of green algae in the cells lining its gut) lacks any physical mechanisms to keep out pathogens – no thick skin, or anything along those lines. But its epithelial cells release antimicrobial chemicals & antiproteinase enzymes when they detect external antigens.

What about plants? They too have innate defence systems, including mechanical barriers against infection – waxy cuticles, and bark (cork), and also the trichomes (hairs) that you find on many leaves – that . But bark can split, & cuticles can be pierced eg by insect mouthparts – what do plants do then? It seems that when plants detect an invading organism, they release high levels of salicylic acid (the active ingredient in aspirin) in the affected tissues. This induces programmed cell death in the affected tissues, which restricts the spread of the pathogen, and also activates immune responses elsewhere in the plant – this in turn means the plant is now primed to resist futher attacks on other tissues. Salicylic acid isn’t the only chemical resonse to infection; it turns out that plants also produce an enzyme called nitric oxide synthase, which catalyses production of nitric oxide (NO) after an infection.

Now, a pathogen that can evade an organism’s immune system for any length of time is going to be at a selective advantage, and so you get a form of arms race, where hosts with the ability to detect & respond to such a pathogen are in turn likely to have better odds of survival, & so on. Some strains of the bacterium Staphylococcus, for example, are able to wrap themselves in strands of the protein fibrin (which they obtain from the host’s blood), which may make them much harder for the host’s immune cells to destroy. (Alas for the patient – this ability is also linked to clotting; Not Good at all.)

Like animals, plants use ‘pathogen-associated molecular patterns’, or PAMPS, as the basis for identifying pathogens (de Jonge et al., 2010), so a pathogen that can somehow hide these from a plant would be at an advantage. The range of potential PAMPS – detected by receptors on the plant cell surface – includes lipopolysaccharides, peptidoglycans, a protein called flagellin, sugars typically found in fungal cell walls – & chitin, a major constituent of cell walls in fungi. Plants with damaging mutations in these receptors would potentially be more susceptible to attack by bacteria & fungi.

De Jonge & his colleagues studied  the cause of leaf mould in tomatoes, a fungus called Cladosporium fulvan. When this fungus is moving into the inside of a leaf, among the proteins it releases is one that protects the fungal cells from plant enzymes called chitinases, which would otherwise break down the fungus cell walls. Actually there’s more to it than that – when chitinases hydrolyse fungal cell walls, this releases molecules that appear to act as PAMPs & so stimulate the plant’s immune defences.

Another protein, called Ecp6, seemed to be needed for the fungus to be really effective at infecting tomato plants. Looking this more closely, the team found that Ecp6 doesn’t affect chitinase release but appears to tidy up other proteins released by the fungus, so that they aren’t floating around & able to be detected by the plant’s defences. So, because the host’s immune system doesn’t kick in, C.fulvan is able to grow more rapidly within the plant’s tissues. And It turns out that the genes controlling Ecp6 production are widespread in fungi – perhaps one outcome of the plant-fungus arms race. (And other example of how plants are considerably more complex than many of us would think.)

de Jonge R, van Esse HP, Kombrink A, Shinya T, Desaki Y, Bours R, van der Krol S, Shibuya N, Joosten MH, & Thomma BP (2010). Conserved fungal LysM effector Ecp6 prevents chitin-triggered immunity in plants. Science (New York, N.Y.), 329 (5994), 953-5 PMID: 20724636

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