# 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 Involved in the Synthesis of SA  
SA is a 7-carbon phenolic acid synthesized via two routes: the isochorismate pathway in the chloroplast and the phenylalanine (Phe) ammonia-lyase pathway. In the chloroplast, chorismate is isomerized to isochorismate synthase (ICS); isochorismate is then converted to SA and pyruvate by isochorismate pyruvate lyase. Gene(s) encoding isochorismate pyruvate lyase in plants have not been identified yet. In _Arabidopsis_, there are two _ICS_ genes: _ICS1_ and _ICS2_[153; 154]. Under pathogen infection or stress conditions, the _ics1_ mutants accumulated -5-10% and the _ics1_ _ics2_ double mutant accumulated -4% of wild-type levels of SA [153; 154]. These genetic studies demonstrated that the isochorismate pathway is the primary route of SA biosynthesis in plants [153; 154]. In the chloroplast, chorismate is also converted to Phe, which is exported to the cytosol [9; 10; 11]. In the cytosol, Phe is converted to cinnamate by Phe ammonia-lyase; cinnamate is then converted to SA via \(\beta\)-oxidation or non-oxidative routes. After synthesis, SA may be modified via glucosylation, methylation, amino acid conjugation, sulfonation, and hydroxylation, which allows fine regulation of its accumulation, activity, and mobility [10; 11]. SA plays regulatory roles in plant growth and development, abiotic stresses, and biotic stresses [10; 11]. The effects of SA treatment on photosynthesis under optimal growth conditions are controversial [155]. Spraying soybean shoots with SA solutions significantly improved plant growth although the photosynthetic rate was not affected [156]. Other researchers reported that foliar application of SA at an optimal concentration (10\({}^{-5}\)\(\upmu\)M) on Indian mustard, maize, and soybean plants resulted in significant increases in photosynthetic rates while SA treatment at higher concentrations had inhibitory effects on photosynthesis [157; 158; 159]. Under stress conditions, pretreatment with SA minimized the detrimental effects of stress factors and thus resulted in higher photosynthetic capacity [160; 161; 162]. Taken together, the effects of SA application on photosynthesis are dependent on plant species, application methods and durations, and growth conditions [155]. The SA-feeding experiments also suggest that delicately regulated SA levels are needed for optimum photosynthesis [155]. A similar conclusion was drawn from physiological characterization of _Arabidopsis_ mutants with constitutively high or low SA contents [163]. Under standard growth conditions, all the mutants displayed suboptimal photosynthesis and a dwarf phenotype [163]. SA and its derivate methyl SA induce local resistance at the site of infection and SAR at the whole-plant level [10; 11]. Examples of SA-induced local resistance include localized cell death and defense gene expression [10; 11]. To develop SAR, a signal from the infected leaf is transmitted to other parts of the plant via the phloem. Recent studies showed that methyl SA acts as a phloem-mobile signal [164]. When the accumulation of methyl SA at primary infected tobacco leaves was suppressed by silencing SA methyl transferase, SAR was compromised [164]. In _Arabidopsis_, SA-induced SAR is primarily mediated by NPR1 (nonexpressor of PR genes 1) [165; 166; 167]. In uninfected plants, NPR1 exists as disulfide-linked oligomers in the cytoplasm [168]. Upon pathogen infection, the increase in SA results in reduction of disulfide bonds in NPR1, monomerization, and subsequent translocation to the nucleus, where NPR1 activates the expression of \(PR\) genes [168]. S-nitrosylation of cysteine (Cys) 156 in NPR1 facilitates its oligomerization and retention in the cytoplasm, whereas disulfide reduction by SA-activated thioredoxin promotes monomerization and nuclear translocation [168]. In rice, SA signaling is branched into the NPR1-dependent and the WRKY45 transcription factor-dependent pathways [169]. Although SA and JA are both classified as defense hormones, they use different strategies against pathogens.