Sunday, 12 February 2012

Running away is not an option, or how plants fight infection

Like animals, plants can be infected by a range of pathogenic organisms. And, like animals, plants possess an immune system to fight off attacks from pathogens. The plant immune system is analogous to the innate immune system in higher eukaryotes but does not involve mobile immune cells such as macrophages. Instead, it is every cell for itself when dealing with a potential infection.

The plant innate immune system recognises molecules common to groups of infecting microorganisms known as microbe-associated molecular patterns (of MAMPs). When surface receptors bind these MAMPs, the immune response responds in a non-specific manner—for example, by inducing production of antimicrobial agents that can protect other parts of the plant, or by initiating cell death in order to prevent spread of an infection.  

Successful pathogens, however, have ways to get around the initial immune response. By injecting effector molecules into the plant cell, they are able to interfere with the cell’s ability to mount an effective response. This has led to the evolution of a second branch of the innate immune system in plants which recognises a pathogen’s effector molecules once they get inside the cell, or responds to the downstream effects of these effectors on the plant cell.
The two branches of the plant innate immune response to a pathogen.

The innate immune system is on the front-line in a plant’s battle against infection, so it needs to be extremely good at recognising invading pathogens. Despite the importance of the innate immune system’s ability to recognise threats, little is known about the range and diversity of the MAMPs capable of triggering the immune response. 

So what makes a good MAMP? Because of the non-specific nature of the innate immune response, it is impossible for the receptors on a plant cell to recognise every protein found in every pathogen. Therefore, the immune system focuses only on those proteins which are commonly found in a range of infectious organisms—these tend to be important proteins with a vital function across many species. But a pathogen has its own ways to avoid being recognised and subsequently killed. One method is to vary those proteins that are recognised by the host’s immune system so that they are no longer detected. For this reason, proteins are under strong positive selective pressure to diversify—natural selection will lead to the evolution of pathogens possessing mutated proteins that are no longer recognised by the host’s immune system. However, the more important a protein, the less likely that a random mutation will be tolerated. So vital proteins are also under strong negative selective pressure to maintain their function.

This paradoxical situation results in different regions of an immune system-recognised protein being under either positive or negative selective pressure depending on whether a mutation in that region disrupts host recognition or destroys protein function. By identifying proteins with this particular pattern of positive and negative selection, a group at the University of Toronto searched the genomes of a number of plant pathogens for potential elicitors of innate immunity and their work was recently published in PNAS.

After screening the genomes for potential immune response elicitors, they synthesised the corresponding peptides and inoculated them into A. thanliana (a species of cress commonly studied by plant biologists). These plants were then challenged with a pathogen to determine if the peptides could suppress virulence, indicating that they had triggered the innate immune response.

In total, the researchers found 55 new peptides capable of switching on the innate immune response. It is hoped that this work will give an insight into how co-evolution of plants and their pathogens has occurred. In addition, understanding how the plant innate immune system works could make it possible to synthesise new antimicrobial agents capable of transiently protecting plants from pathogens, or even to genetically engineer improved plants with better disease resistance.

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