Abiotic stress-induced chloroplast proteome remodelling: a mechanistic overview.

The chloroplast houses photosynthesis in all green plants, and is therefore of fundamental importance to the viability and productivity of plants, ecosystems, and agriculture. Chloroplasts are, however, extremely vulnerable to environmental stress, on account of the inherent volatility of oxygenic photosynthesis. To counteract this sensitivity, sophisticated systems of chloroplast stress acclimation have evolved, and many of these involve broad proteome changes. Here, we provide an overview of the interlocking and mutually dependent mechanisms of abiotic stress-induced chloroplast proteome remodelling. Topics that are covered in this context include: nucleus to chloroplast signalling mechanisms, with a particular emphasis on the nuclear control of the chloroplast genome; chloroplast to nucleus signalling; and the roles of chloroplast pre-protein import regulation and chloroplast proteases.

The role of chloroplasts in plant pathology.

Plants have evolved complex tolerance systems to survive abiotic and biotic stresses. Central to these programmes is a sophisticated conversation of signals between the chloroplast and the nucleus. In this review, we examine the antagonism between abiotic stress tolerance (AST) and immunity: we propose that to generate immunogenic signals, plants must disable AST systems, in particular those that manage reactive oxygen species (ROS), while the pathogen seeks to reactivate or enhance those systems to achieve virulence. By boosting host systems of AST, pathogens trick the plant into suppressing chloroplast immunogenic signals and steer the host into making an inappropriate immune response. Pathogens disrupt chloroplast function, both transcriptionally-by secreting effectors that alter host gene expression by interacting with defence-related kinase cascades, with transcription factors, or with promoters themselves-and post-transcriptionally, by delivering effectors that enter the chloroplast or alter the localization of host proteins to change chloroplast activities. These mechanisms reconfigure the chloroplast proteome and chloroplast-originating immunogenic signals in order to promote infection.