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Petra Boevink

Staff picture: Petra Boevink
Cell and Molecular Sciences
Cell and Molecular Sciences
Cell / Molecular Biologist
petra.boevink@hutton.ac.uk
+44 (0)344 928 5428 (*)

The James Hutton Institute
Invergowrie
Dundee DD2 5DA
Scotland UK

 

Current research interests

The focus of my research is the cell biology of plant-pathogen interactions, in particular between the notorious oomycete pathogen Phytophthora infestans, the causal agent of the devastating potato late blight, and its hosts. This pathogen manipulates plant defence responses on multiple levels, suggesting complex exchanges of signals between host and pathogen and a variety of effector functions. I work closely with Paul Birch (of Dundee University Plant Sciences, based at the James Hutton Institute) and Steve Whisson and other members of the strong Phytophthora team in Dundee and we are part of the Dundee Effector Consortium which encourages collaboration and exchange between teams working on different pathogen/pest-plant interactions. 

The biotrophic phase of growth is an essential step in the P. infestans infection process. It represents a point of vulnerability and is the stage at which the pathogen must exert the most control over the host responses. The formation of haustoria is crucial for the establishment of the biotrophic phase by P. infestans. A transmembrane protein, PiHMP1, is essential for infection and specifically localises to haustoria during infection. It has proven to be a particularly useful marker for the biotrophic stage.

A key focus of the P. infestans group, which is composed of both University of Dundee and James Hutton Institute staff, has been on characterising the activities of the RXLR effector repertoire and how the targeted host pathways contribute to pathogen defence and infection development. The P. infestans genome encodes hundreds of genes for small, secreted RXLR (+/-EER) (a conserved motif similar to the one involved in protein translocation in the malaria parasite) proteins. All known oomycete pathogenicity effectors that are recognised by cytoplasmic plant resistance proteins (and are thus referred to as avriulences; Avr's) contain RXLR motifs. We have prioritised about 200 of these effectors based on expression patterns, recognition, silencing phenotypes, etc. for further study. The aims of our BBSRC Lola grant (2009-2014) in collaboration with Jim Beynon's team at Warwick University were to characterise RXLR effectors from P. infestans and another oomycete, H. arabidopsidis. Many of the RXLR effectors were implicated in suppressing plant defences by their putative targets. We have since confirmed that this is indeed the case for several RXLR effectors.

We focussed on effectors that appeared to be most important, interesting and tractable for further work. What has been revealed by effector studies is the great breadth of the pathogen's activities in the host. PiAVR3a, an essential effector, has 14 candidate host protein interactions. The complexities of the interaction between PiAVR3a and the E3 ligase CMPG1 alone took several years to unravel. There is more work to be done to fully understand PiAVR3a's essential roles in infection. PiAVR3a has provided other interesting stories. The NBS-LRR receptor R3a relocates to endosomal compartments when co-expressed with the recognised form of PiAVR3a (KI) and this relocation is required for its signalling activity. This behaviour was also seen in the R3a variants that were shuffled and selected for detection of the normally undetected EM form of PiAVR3a.

The nuclear-targeted effector Pi04314, one of the most highly expressed effectors and one that gives a large boost to P. infestans infection when co-expressed in leaves, binds to isoforms of the protein phosphatase type 1 catalytic domain (PP1c) and forms a host-pathogen holoenzyme, exploiting the phosphatase activity to benefit infection. Similarly nucleolar-associated effector Pi04089 exploits the activity of a KH type of RNA binding protein (StKRBP1), Pi02860 targets a predicted potato E3 ligase NPH3/RPT2-like 1 (StNRL1) and Pi17316 uses MAP3K StVIK1. Thus StPP1c's the StKRBP1, StNRL1 and StVIK1 are all susceptibility factors and the potential S factors as novel targets for development of plant resistance is being investigated in a BBSRC IPA-funded project.

PiAVR3a is detected by R3a within the plant cell cytosol and the RXLR-EER motif is required for the recognition. The motif is required for translocation of PiAVR3a into the plant cytosol. RFP-tagged PiAVR3a was the first tagged RXLR effector to be expressed in the pathogen and it localised to the haustoria during infection. Several other RXLR effectors have since been expressed in Phytophthora, such as PiAVR2, Pi04314 and Pi22926, and these also concentrate at haustoria suggesting that haustoria play a major role in suppression of plant defences. Indeed, not only RXLR effectors concentrate at haustoria, pathogenicity proteins that function in the extracellular space were also found to be secreted most strongly at haustoria. Inhibitor studies have revealed that apolastic effectors and other pathogenicity proteins are conventionally secreted while the translocated RXLR efectors are secreted by a different pathway, i.e. they are non-conventionally secreted. We are investigating how RXLR effectors are targeted to the non-conventional route and how that results in them being translocated into host cells.

The imaging and cell biology facilites and capabilites at The James Hutton Institute are managed by Alison Roberts, Kath Wright and Sean Chapman in addition to their own research activities. High quality imaging work is not possible without great training, ongoing support and facility management.


Printed from /staff/petra-boevink on 19/09/19 08:22:53 PM

The James Hutton Research Institute is the result of the merger in April 2011 of MLURI and SCRI. This merger formed a new powerhouse for research into food, land use, and climate change.