Abiotic and biotic challenges pose serious risks to plant growth and crop production world-wide. The plant hormone Jasmonate (JA) is essential to protect plants against insect herbivory, mechanical wounding and necrotrophic pathogens. Upon these challenges, JA hormone levels increase and induce defense responses while stunting growth. Hence, understanding how plants balance growth-defense trade-offs during environmental stresses represents a tremendous opportunity to improve plant yield and meet the global need for increased food production. Through an extensive genetic approach in the model plant Arabidopsis thaliana, the host lab has identified PLEIOTROPIC REGULATORY LOCUS 1 (PRL1) as new putative regulator of the JA pathway. PRL1 is also known for its role in sugar signalling and metabolism, representing a probable integration node for balancing growth during stress responses. This project thus aims to characterize the role of PRL1 in activating the JA pathway and uncover how are sugar and defense signalling integrated during insect and fungal attacks. Specifically, I will use state-of-the-art cell biology, biochemistry and molecular biology approaches available at the host institute to answer the following questions: 1. How does PRL1 regulate JA responses? 2. How does PRL1 impact cell-type specific JA-mediated defense strategies? 3. How are PRL1- and JA-signalling pathways integrated? 4. What is the role of PRL1 in plant defense responses against insect herbivory and fungal pathogens? In addition to increasing our fundamental understanding of plant-pathogen interactions and activation of hormonal pathways, this ambitious project will inevitably provide novel targets and strategies to improve crop adaptability and secure means for stabilizing future food security.

Plants evolved diverse strategies, including the production of specialized metabolites to adapt to changing environments. These specialized metabolites are often linked to glandular trichomes (GTs) density. To study GT’s biology, cultivated tomato and their wild relatives are considered ideal models, varying in GT types (I, IV, VI, VII) and associated metabolites. While type IV GTs, rich in acyl sugars (AS), persist throughout the life cycle of wild tomatoes, in cultivated varieties, they explicitly appear in early stages (especially on hypocotyl and cotyledons). AS provides resistance to various pathogens, including whiteflies, a significant threat to global tomato production. Although the role of type IV GTs and AS in adult plant resilience is understood, their regulation at the juvenile stage remains unknown. This study aims to address these knowledge gaps, employing an integrative OMICS approach in the early developmental stages of cultivated tomato and their wild relatives. While factor like plant hormone jasmonic acid (JA) is known to influence the development of type VI GTs and terpenoid metabolism, the JA-mediated regulation of type IV GTs and AS metabolism remains unidentified. The present proposal aims to tackle these crucial knowledge gaps by utilizing combinatorial forward and reverse genetics approaches. Furthermore, this project aims to explore the ecological functions of type IV GTs and AS in shaping the plant microbiome at the cotyledon stage, a yet unknown aspect of plant fate. Through an interdisciplinary approach, including genetics, transcriptomics, metabolomics, and microbiome analysis, the research aims to offer comprehensive insights into plant defense mechanisms and adaptation strategies in early developmental stages. The outcomes of this research will revolutionize our understanding of plant resilience at juvenile stages, thereby contributing to the progress of sustainable agriculture and offering new opportunities for crop improvement.

Both animals and plants produce potently active mediators in response to tissue injury. These oxygenated lipid derivatives include leukotrienes and prostaglandins in animals, and jasmonates (JAs) in plants with JA-Ile serving as the bioactive phytohormone in angiosperms. JAs are synthesized from poly unsaturated fatty acids residing in plant-specific plastidial membranes, and are essential to protect plants against numerous biotic and abiotic challenges including insect herbivory and temperature extremes. Despite the vital roles of JAs in sustaining plant fitness and although JA-Ile biosynthesis and signalling are well characterized, it is still unknown how are damage signals transmitted to plastids to initiate phytohormone production and what is the nature of the transmitted signal(s). Our previous work in Arabidopsis uncovered that osmotically-induced turgor pressure changes elicit JA-Ile biosynthesis. We hence hypothesise that JA-Ile biosynthesis initiation may result from the transmission of mechanical signals through tissues and cell compartments leading to biophysical changes of plastidial membranes granting substrate accessibility to JA biosynthesis enzymes. To address these central questions in plant biology we aim to: 1. Quantify the mechanical forces and osmotic pressure changes required to induce JA biosynthesis 2. Characterize cellular events that transduce mechanical and osmotic stress signals to plastids for JA-Ile precursor production 3. Alter plastidial biophysical parameters and study the consequences on JA-Ile precursor production 4. Identify genetic components involved in sensing and decoding biophysical stimuli for JA-Ile production This proposal thus intends to fill a critical gap in knowledge on stress phytohormone biology regulating plant acclimation and, concomitantly, expand our understanding on fundamental aspects of plant mechano- and osmo-sensing.

This is a joint project between the James Hutton Institute (JHI, formerly SCRI) and Rothamsted Research (RRes) that focuses on the "Combating pests and diseases" research challenge highlighted by the industrial members of the Crop Improvement Research Club (CIRC). It is addressing one of the highlighted areas for the second CIRC call: Crop protection. Two teams with complementary expertise in different areas of plant science will combine efforts in exploiting pathogen genome sequence. We aim to advance fundamental understanding of plant immune responses and identify novel sources of resistance to the most economically important barley fungal pathogen Rhynchosporium commune (Rc), formerly known as R. secalis. Rc can cause yield losses of up to 40% and reduce grain quality. Populations of Rc can change rapidly, defeating new barley resistance (R) genes and fungicides after just a few seasons of their widespread commercial use. New EU regulations may lead to loss of the most effective triazole fungicides, making Rc control even more problematic. All pathogens trigger non-host resistance (NHR) in plants. Successful pathogens can suppress or manipulate NHR by secretion of small proteins called 'effectors'. Once a pathogen has suppressed NHR, plants deploy a second layer of defence in the form of R proteins. R proteins detect certain pathogen effectors, termed 'avirulence' (Avr) proteins, and activate resistance responses. Pathogens can avoid recognition by some of the R proteins by losing either the expression or function of a non-essential (redundant) effector with no apparent cost to pathogen fitness. Both of these strategies have been deployed by Rc, mutating or eliminating AvrRrs1, to completely overcome Rrs1-mediated resistance in under 10 years. We aim to understand redundancy within Rc effectors. R proteins recognising non-essential effectors are not durable. Therefore breeding should aim to target introgression of R genes recognising essential effectors that are less variable in pathogen populations. This effector type has been found for other fungal and oomycete plant pathogens. Rc genome sequencing has provided a unique opportunity to identify the putative effector repertoire. Comparison of genome sequences of 9 Rc strains that are able to overcome different R genes will allow rapid prediction of candidate effectors that are less variable in Rc populations, and therefore are more likely to be indispensable. RNA sequencing of Rc germinated conidia and barley leaves infected with Rc provides important information about predicted effectors expressed during the onset of infection. Expression of less variable candidate Rc effectors will be assessed throughout the infection. Based on expression profiles, degree of conservation between the strains, and the ability to induce cell death in one or more barley genotype, 25 predicted effectors will be chosen for targeted gene disruption to identify those essential for fungal pathogenicity. The RRes team has recently developed an efficient system for screening barley germplasm for recognition of Rc effectors. It is based on systemic expression of Rc small secreted proteins in barley leaves using a plant virus as a delivery vector. This method can be extended to other cereals, including wheat, and their pathogens. The extensive JHI collection of barley cultivars, landraces and mapping populations will be screened to (1) identify novel sources of distinct and potentially durable resistances to Rc, which can be combined to increase the durability of resistance, and (2) characterise resistance already present in current breeding material. This will have direct positive impact on Rc disease resistance breeding programmes. Deployment of this resistance will stably increase yield and quality of new barley cultivars, while reducing fungicide use, greenhouse gas emissions and environmental pollution.