Investigating the influence of phytopathogenic effectors upon host transcription

Phytopathogens have developed methods to suppress, manipulate and avoid host defences though the production of toxins and proteins that act on the exterior and interior of host cells. Pathogenic proteins that promote susceptibility to the pathogen are termed effectors, and can function through the suppression of host defences and the diversion of host nutrients. Plants are able to detect select effectors, and thus regain resistance. This multilayered defence response and diverse array of pathogenic effectors can cause the outcome of infection to be decided by a single protein from either organism. Current characterised effectors are able to block pathogen-associated molecular pattern recognition, downstream signalling, up-regulate susceptibility genes including nutrient transporters, modify chromatin structure, interfere with RNA metabolism, suppress or prevent effector-triggered immunity and block the defensive and culminating plant cell death. Research conducted here aims to investigate the in uence of effectors from two pathogens upon transcription in their common host, Arabidopsis thaliana. Over 30 Pseudomonas syringae pv. tomato (Pst) DC3000 effectors, which are delivered directly into the host cell, have been at least partially characterised with several more predicted from the sequenced genome. The research presented here analyses a high resolution microarray time series dataset, comparing the transcriptional events that take place during virulent Pst DC3000 infection to infection with an avirulent mutant that is unable to deliver effectors into the host cell; Pst HrpA