# Chloroplasts at the Crossroad of Photosynthesis, Pathogen Infection and Plant Defense
## 2 The Chloroplast is a Major Synthesis Site for Many Plant Hormones
### The Chloroplast is also a Site of JA Synthesis  
JA is a 12-carbon oxygenated fatty acid derivative, subsequently synthesized in chloroplasts and peroxises [7; 8]. In the chloroplast, the 18-carbon fatty acid linolenic acid (18:3) is released from membrane lipids and then oxidized at the C-13 position by a lipoxygenase. This reaction requires O\({}_{2}\) as a substrate. The oxidized intermediate is cyclized into 12-oxo-phytodienoic acid (OPDA) by the combined action of allene oxide synthase and allene oxide cyclase. After being transported to the peroxisome, OPDA is reduced into 3-oxo-2-(2-pentenyl)-cyclopentane-1-octanoic acid (OPC-8) by OPDA reductase. This reaction consumes NADPH. OPC-8 is then converted to JA via \(\beta\)-oxidation, which requires the participation of ATP and O\({}_{2}\). Once synthesized, JA may undergo amino acid conjugation, methylation, sulfonation, glucagonylation, and hydroxylation [8]. These chemical modifications allow fine-tuning of the accumulation, activity, and mobility of JA [8]. JA also is a regulator of plant growth and development, abiotic stresses, and biotic stresses [7; 8]. Exogenous treatment of potato leaves with 1 uM JA caused significant reduction in the amounts of photosynthetic pigments [137]. Furthermore, methyl JA-treated _Arabidopsis_ protoplasts as well as _Vicia fuba_ and rice seedlings displayed compromised photosynthetic electron transport and carbon fixation reactions [138]. These photosynthetic defects were attributed to ROS accumulation as pre-incubation of samples with an antioxidant or ROS scavenger offered significant protection [138]. JA is involved in defense against necrotrophic pathogens and herbivous insects [7; 8]. JA and ET act synergistically upon attack by necrotrophs; JA and ABA act synergistically during herbivory [7; 8]. Necrotrophic pathogen attacks induce the expression of JA- and ET-responsive genes and defense against these pathogens [7; 8]. Methyl JA treatment was found to up-regulate the expression of genes in JA biosynthesis, defense responses, oxidative stress responses, senescence, and cell wall modification, and down-regulate the expression of genes in chlorophyll biosynthesis and photosynthesis [139]. This general trend was also observed at the protein level [140]. JA is also a central player in induced systematic resistance (ISR), which is induced by nonpathogenic microbes, such as plant growth-promoting rhizobacteria and mycorrhiza, upon root colonization [134]. ISR confers a broad spectrum of resistance to future pathogen invasion in many plant species [134]. ISR was blocked in _Arabidopsis_ JA-signaling mutants [141; 142; 143], demonstrating the role of JA in ISR. JA influences the production and signaling of other hormones (Figure 1). JA may exert positive impacts on ABA signaling under abiotic stress. For example, JA application caused increased ABA levels in barley and citrus seedlings [144]. JA accumulation appeared to be needed for ABA build-up under drought conditions [145; 146], consistent with the notion that ABA and JA act synergistically under drought [147]. As mentioned previously, JA and ABA act synergistically on the MYC branch of JA signaling to activate wounding-responsive genes and repress pathogen-responsive genes while JA and ET act synergistically on the ERF branch to activate pathogen-responsive genes and repress wounding-responsive genes [91; 92]. Furthermore, depending on the plant species and growth stage, methyl JA application may promote or inhibit ET production in seedlings, fruits, and seeds [148]. JA influences the production and signal transduction of non-hormone signaling molecules (Figure 1). For example, methyl JA treatment caused sequential increases of mitochondrial and chloroplastic H\({}_{2}\)O\({}_{2}\) in _Arabidopsis_ protoplasts, which led to mitochondrial aggregation and swelling, photosynthetic dysfunction, chloroplast morphology changes, and ultimately, cell death [138]. Methyl JA-induced H\({}_{2}\)O\({}_{2}\) accumulation was also observed in guard cells and intact seedlings [138; 149].