Visible light is the basic energetic driver of plant biomass production through photosynthesis. The constantly fluctuating availability of light and other environmental factors means that the photosynthetic apparatus must be able to operate in a dynamic fashion appropriate to the prevailing conditions. Dynamic regulation is achieved through an array of homeostatic control mechanisms that both respond to and influence cellular energy and reductant status. In addition, light availability and quality are continuously monitored by plants through photoreceptors. Outside the laboratory growth room, it is within the context of complex changes in energy and signalling status that plants must regulate pathways to deal with biotic challenges, and this can be influenced by changes in the highly energetic photosynthetic pathways and in the turnover of the photosynthetic machinery. Because of this, defence responses are neither simple nor easily predictable, but rather conditioned by the nutritional and signalling status of the plant cell. This review discusses recent data and emerging concepts of how recognized defence pathways interact with and are influenced by light-dependent processes. Particular emphasis is placed on the potential roles of the chloroplast, photorespiration, and photoreceptor-associated pathways in regulating the outcome of interactions between plants and pathogenic organisms.

SummaryOxidative stress responses are influenced by growth day length, but little is known about how this occurs. A combined reverse genetics, metabolomics and proteomics approach was used to address this question in Arabidopsis thaliana.A catalase-deficient mutant (cat2), in which intracellular oxidative stress drives pathogenesis-related responses in a day length-dependent manner, was crossed with a knockdown mutant for a specific type 2A protein phosphatase subunit (pp2a-b′c). In long days (LD), the pp2a-b′c mutation reinforced cat2-triggered pathogenesis responses.In short days (SD), conditions in which pathogenesis-related responses were not activated in cat2, the additional presence of the pp2a-b′c mutation allowed lesion formation, PATHOGENESIS-RELATED GENE1 (PR1) induction, salicylic acid (SA) and phytoalexin accumulation and the establishment of metabolite profiles that were otherwise observed in cat2 only in LD. Lesion formation in cat2 pp2a-b′c in SD was genetically dependent on SA synthesis, and was associated with decreased PHYTOCHROME A transcripts. Phosphoproteomic analyses revealed that several potential protein targets accumulated in the double mutant, including recognized players in pathogenesis and key enzymes of primary metabolism.We conclude that the cat2 and pp2a-b′c mutations interact synergistically, and that PP2A-B ′c is an important player in controlling day length-dependent responses to intracellular oxidative stress, possibly through phytochrome-linked pathways.