Research Interests

The world population is predicted to reach 9.7 billion by 2050, compared to today's 8.0 billion. More food needs to be produced from ever-dwindling natural resources with the additional challenges arising from climate change. The UK imports 45% of all its food and so future food security is both a global and a national issue that needs urgently addressing. One key approach is to reduce waste in the food chain. Between 17-30% of global crops are lost to pests and disease both pre- and post-harvest. The big challenge is therefore to breed crops with enhanced tolerance to plant pathogens but, crucially, without adversely compromising yield.

The endoplasmic reticulum (ER) is a major protein and lipid factory present in every plant cell. It forms a mesh-like network of membrane tubules and sheets, which extends throughout the cell and between nearby cells and is constantly reshaping and reorganising to meet the cells' changing demand for proteins. However, despite its "lace-like" appearance being first described in detail in 1945 (doi: 10.1084/jem.81.3.233), little is known about the fundamental relationship between the intricate form of the ER and its function. Focusing on the plant ER, my research asks how cellular perturbations caused by exposure to pathogens impact on this ER form-function relationship and, ultimately, on the ability of the plant to produce an effective and timely immune response.

We have recently discovered that when Arabidopsis leaves are infected by the bacterial pathogen Pseudomonas syringae pv.tomato DC3000, the ER network undergoes dramatic and rapid reorganisation, which is necessary for pathogen proliferation. Crucially, these changes to the ER's shape and movement occur on a cell-autonomous basis, with some cells in the immediate vicinity of DC3000 showing striking ER alterations but other cells appearing completely unaffected. These alterations to the ER require the secretion of effector molecules into the plant cell. A few pathogen effectors are known to target the ER either directly or indirectly, but little is known about their modus operandi in promoting disease. We have also discovered that Arabidopsis mutants with altered expression of key ER morphogenic proteins display very significant differences in their susceptibility to DC3000, further indicating that regulation of ER morphology is a key battleground during pathogen infection.

My current research aims to elucidate how ER architecture is remodelled by DC3000 and which specific effectors are involved in this process, with the ultimate aim of applying this information, together with our existing toolkit of ER-shaping proteins, to engineer 'smart' plants that are able to rapidly alter their ER architectural dynamics in response to biotic perturbations. Through an ongoing collaboration with Professor Mark Fricker (University of Oxford) we are performing quantitative multivariate analysis of ER architecture and dynamics from high-resolution confocal microscopy images using our bespoke AnalyzER computational pipeline which is capable of capturing even subtle changes in ER structure or behaviour with statistical rigour.

In addition to its core role in the biosynthesis, folding and quality control of secretory and membrane proteins, the pervasive nature of the ER make it ideally suited as a conduit for intra-organellular signalling. I am therefore also interested in understanding the wider role of the ER in coordinating the cellular response to environmental stress.