Chloroplasts – a new effector battleground?

Successful pathogens attenuate a battery of sophisticated plant surveillance defences by deploying a collection of “effector” molecules, the majority of which are function redundantly in planta, targeting multiple levels and nodes of an activated innate immune signalling network. We have made remarkable progress towards understanding how molecular patterns of potential pathogens are recognised by pattern recognition receptor complexes at the host-pathogen interface to activate a kinase signalling cascade leading to transcriptional re-programming that underpins plant innate immunity. Early transcriptional events occur within 30 min of Pseudomonas infection, but the pathogen does not multiply until 7-8 hpi. Our knowledge of the core host physiological processes modified by multiple effectors to promote virulence, remains rudimentary. High-resolution microarray time courses of a compatible infection of Arabidopsis with P. syringae pv. tomato DC3000 and the disarmed hrpA mutant combined with genetic, physiological and real-time imaging studies revealed that the chloroplast, a key organelle in primary carbon metabolism and site of synthesis of hormone precursors, is rapidly targeted by bacterial effectors. Within 2hpi of DC3000 or hrpA challenge, ~20% of all differentially suppressed transcripts are nuclear encoded chloroplast targeted genes (NECG) subsequently exceeding 35%. Within 3hpi effectors reprogramme NECG transcription. We show that many effectors have potential chloroplast targeting sequences and these can translocate to chloroplasts, where they attenuate a MAMP activated chloroplast reactive oxygen burst, probably through elevation of ABA. Attenuation of the oxidative burst by exogenous application of DCMU allows growth of the hrpA mutant. This talk with discuss our progress towards understanding chloroplast immunity.