| Summary: | Plants are fundamental to life on Earth, especially for the role they play in the food chain. With the world human population predicted to exceed 9 billion by 2050 the pressure on our agricultural system is set to increase. Not only does agriculture have to expand in order to feed this ever growing population it also needs to effectively deal with the threat that plant pathogens pose to food security. The relationship between plants and their pathogens is immensely complex, with subtle differences at the molecular level defining whether a host becomes infected or remains healthy. These molecular differences are exemplified by pathogen effectors that manipulate processes inside the host cell to benefit colonisation. Knowledge of how these effectors and their targets function is crucial to develop strategies to enhance crop resistance. This project focuses on one such effector, Pi17316, which is secreted by the potato late blight pathogen, Phytophthora infestans, to target a host MAP3K, VIK. Inside the plant cell Pi17316 localises to the plasma membrane, where it interacts with VIK in order to suppress the INF1 and R2/Avr2 cell death pathways and to enhance P. infestans colonisation. VIK itself was shown to be a susceptibility factor, required for full P. infestans colonisation. Overexpression of StVIK results in the suppression of INF1 and R2/Avr2 responses and enhances P. infestans ability to colonise the host. Furthermore, silencing of NbVIK attenuates infection and negates any positive effect on colonisation that Pi17316 provides, demonstrating that VIK activity is required for disease. Here it is shown that Pi17316 requires plasma membrane localisation and the presence of VIK in the host in order to suppress the INF1 and R2/Avr2 pathways to promote P. infestans colonisation.
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