Biotic stress contributes disproportionately to crop losses, accounting for in excess of 25% of global yield. Thus, developing novel approaches to restricting pathogen infections of crops and consequently improving yields must be a key future objective for food security.
Plants deploy two main immune defence pathways. Plants initially perceive pathogens via surface receptors that recognise non-self, or Pathogen Associated Molecular Patterns or PAMPs. This is termed PAMP Triggered Immunity, or PTI. Pathogens deliver effectors into the cell which both suppress PTI and reconfigure host cells to provide a favourable environment for pathogen multiplication. R proteins are primarily intracellular receptors which perceive these pathogen effectors to confer Effector Triggered Immunity (ETI) by either direct interaction, or indirectly initiating the hypersensitive response (HR), a form of programmed cell death. Recent studies suggest that these pathways are not exclusive and mutually potentiate immune responses.
Unfortunately, R-gene mediated resistance, the primary target of plant breeders, is often overcome in the field. This is due to strong selective pressure driving pathogens to rapidly adapt and evolve sophisticated ways of avoiding detection.
The majority of work in the plant-pathogen field focusses on PTI and ETI and few groups look at HOW the pathogen manipulates the host at the cellular level. Effectors collaborate to cause disease, with each providing an incremental contribution to successful infections. Effectors target different organelles, not just the nucleus and cell membrane. Currently our knowledge of how pathogens target cellular organelles and how these inter-organellular interactions are choregraphed to ultimately result in successful infections are poorly understood. Several years ago the Grant lab, using the Arabidopsis thaliana – Pseudomonas syringae pathosystem, demonstrated that chloroplasts are key targets of pathogen effectors and hence the field of “chloroplast immunity” developed. We later showed a role for the Endoplasmic Reticulum (ER) in plant immunity. However, our unpublished results implicate that all major organelles contribute to plant disease progression.
In collaboration with the McKenna lab we have been developing a suite of state-of-the-art imaging resources that will allow us to undertake a detailed, quantitative study of inter-organelle dynamics during P. syrinage infection. Moreover, we have the capacity to visualise across scales, from whole plant imaging of propagating signalling events to subcellular changes in organelle dynamics. We have a large number of dual organelle reporter lines which will allow us to determine how multiple organelles interact with each other and their dynamics during host-pathogen interactions. Additionally, we have several reporter lines for different signalling molecules, including secondary messengers such as Ca2+, targeted to different organelles. This will allow us to not only determine how organelles interact but also the molecular signalling between different organelles during pathogen interactions. This work is underpinned by several advanced imaging technologies from long-term imaging of whole plants to structured illumination microscopy providing unprecedented spatial and temporal resolution. These techniques are readily used in the supervisor’s laboratory.
The successful candidate will receive training and become proficient in plant pathology and cell biology including techniques such as molecular cloning including multigene assembly, confocal and structured illumination microscopy (SIM).
- Microbiology & plant pathology
- Plant Molecular Biology
- Targeted analytical chemistry (mass spectrometry)
- Genetically encoded reporter analysis & whole plant imaging
- Proteomics (including proximity labelling) and RNA-seq
- Advanced Live cell microscopy (confocal, SIM)
- Quantitative Image Analysis
Principal Supervisor: Professor Murray Grant
Secondary Supervisor(s): Dr Joe McKenna
University of Registration: University of Warwick
BBSRC Research Themes:
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