Parasitic plants infect other plants, including food crops, threatening food security. Parasitic plants use a specialised infection organ, the haustorium, to grow into their host plants, establish a vascular connection and exploit the host for water and nutrients. Effective protection against parasitic plants is currently lacking. Cuscuta campestris is a model system for parasitic plants due to its sequenced genome. It infects >170 host plants (including tomato, soybean, potato and sunflower), causing e.g. 50-75% reduction in tomato yields. Cuscuta occurs worldwide in tropical to temperate regions, including France and Southern Scandinavia, and, in the face of climate change, is expected to expand its habitat even further. Polygalacturonases (PGs) degrade homogalacturonan and are essentially required during plant infection by pathogens. C. campestris possesses 65 putative PGs, of which several are specifically expressed in the haustorium with their specific functions unknown. Upon pathogen attack, host plants perceive cell wall breakdown products and pathogen PGs, which trigger defense responses including production of PG-inhibiting proteins (PGIPs).
Using the available genome and transcriptome data we will generate a comprehensive overview of the genes encoding the relevant C. campestris pectin hydrolytic enzymes. It is a logical assumption that part of the genes will encode enzymes for degradation of the host cell wall, tentatively under control of PGIPs to fine-tune enzyme specificity and action. Based on the overview generated the project partners will select a small number of Cuscuta PGs and PGIPs for piloting biochemical characterisation. We will then proceed to unravel the structural and biochemical specificities of PGs and PGIPs from Cuscuta and their putative co-evolution with endogenous (from parasitic plant) or exogenous PGs (from host plant or pathogens). This knowledge generated can identify novel targets for future host plant protection.