In contrast to mammals, plants do not have mobile defender cells and an adaptive immune system; they defend themselves against attack from pathogens using an innate immune system. This immune system relies on the detection of foreign molecules and responds to these in different ways. One such way is the Hypersensitive Response (HR) where plant host cells undergo localised cell death. This makes it challenging for invading pathogens to establish a successful infection. HR is normally observed as a reaction to the presence of translocated effector proteins, which the pathogen has deployed to dampen signalling by other plant immunity pathways that are attempting to resist the invader.
In order to get a deeper insight into this ‘molecular warfare’, researchers from the Sainsbury Laboratory and the John Innes Centre in Norwich investigated a well-known plant-pathogen ‘model’ system namely the plant Arabidopsis thaliana (thale cress) and the bacteria Pseudomonas syringae, which can also cause diseases like bacterial speck or canker in important crop species (e.g. tomato).
The researchers uncovered the three-dimensional crystal structure of an active part of the effector protein ‘AvrRps4’ and used this to investigate protein activity. Certain strains of
P. syringae directly inject AvrRps4 into plant cells, presumably to undermine host defences. Its crystal structure was solved using Diamond beamlines I02 and I04 and additional mutagenesis studies helped to deliver previously unknown aspects of AvrRps4 function.
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The AvrRps4 structure is an antiparallel α-helical coiled coil.(left) Cartoon representation of the α-helices with important residues in sticks (right) Electrostatic surface representation with a prominent negative patch highlighted by the arrow.
To defend against pathogen invasion plants, including Arabidopsis, use two distinct layers of immunity. The first layer involves Pathogen Associated Molecular Patterns (PAMP)-triggered immunity (PTI). PTI is activated by the recognition of PAMPs, ubiquitous molecular signatures that are indispensible for pathogens. The main function of PTI is to prevent further colonization by the invader and PTI pathways are prime targets for the action of effectors. The second layer of immunity, known as effector-triggered immunity (ETI), is the result of recognition of translocated effectors by intracellular immune receptors. AvRps4 is recognised by the plant receptor RPS4 (Resistance to Pseudomonas syringae 4), triggering HR. It is the activation of ETI by AvrRps4 (avr stands for avirulence) that the researchers have focussed on in their study. The antiparallel α-helical coiled coil revealed by the AvrRps4 crystal structure served as a template for mutagenesis to define regions of the protein important for recognition by the RPS4 molecule and a second RPS4-independent recognition event.
The study, which was published in PNAS (online September 17, 2012), adds further details to the unsolved problem how intracellular plant immune receptors activate defence upon effector detection. A thorough understanding, at the molecular level, of how these plant defence pathways are activated in response to pathogens is an important step towards delivering sustainable disease resistance in important crop species.
aThe Sainsbury Laboratory, Norwich Research Park, Norwich NR4 7UH
bDepartment of Biological Chemistry, The John Innes Centre, Norwich Research Park, Norwich NR4 7UH,
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