# Chloroplasts at the Crossroad of Photosynthesis, Pathogen Infection and Plant Defense
## 6 The Participation of Different Plant Signals in Plant Defense against Pathogens  
Phytohormones ABA, ET, JA, and SA, as well as ROS, \(\cdot\)NO, and Ca\({}^{2+}\) directly or indirectly participate in plant defense against pathogens (Figure 2). ABA and ET may have positive and negative impacts on plant defense responses [6, 82]. On the one hand, ABA induces stomatal closure and therefore blocks the entry of bacterial pathogens into plant tissues [28, 29]. On the other hand, ABA has negative impacts on the post-invasion PTI response of plants [83, 84]. Generally, ET inhibits the development of symptoms caused by necrotrophs and enhances the cell death caused by biotrophs and hemibiotrophs [125, 126, 127]. JA and SA have positive impacts on plant defense responses. JA is required in defense against necrotrophs and insect herbivores, and it acts synergistically with other hormones: JA and ET act synergistically against attacks by necrotrophs; JA and ABA act synergistically during herbivory [7, 8]. SA mainly induces resistance to biotrophs and hemibiotrophs [10, 11]. ROS, \(\cdot\)NO, and Ca\({}^{2+}\) spikes generally play positive roles in plant defense against pathogens. The biphasic ROS accumulation is essential for plants to recognize pathogens, execute the hypersensitive response, and minimize the spread of pathogens [193]. \(\cdot\)NO potentiates ROS-induced localized cell death and induces the expression of defense-related genes [258]. Ca\({}^{2+}\) spikes are involved in the development of both PTI and ETI responses [276].  
PAMP Perception Induces Transcriptional Reprogramming of Nuclear-encoded Chloroplast-targeted Protein Genes  
Plant pathogens elicit PAMPs, which are conserved among a particular class of microbes (e.g., flagella for bacterial pathogens and chitin for fungal pathogens) but are not produced by plants. The chemical nature of PAMPs could be polysaccharides, lipopolysaccharideacharides, proteins, glycoproteins, and lipophilic substances [294]. Plants recognize these \"non-self\" molecules by pattern recognition receptors on the cell surface [295]. PAMP (e.g., flagellin and lipopolysaccharideacharides) treatments were found to induce local and systemic SA accumulation and defense gene (e.g., \(PR\) genes) expression in _Arabidopsis_ plants [296]. Further investigations showed that PAMP-induced SA accumulation requires functional ICS1, the key SA biosynthetic enzyme in the chloroplast, and that disruption of SA signaling significantly affected PAMP-triggered defense responses [297]. Researchers inoculated _Arabidopsis_ leaves with \(Pst\) DC3000, T3 SS-deficient mutant strains, and mock solution, and perform comparative transcriptome analysis at a series of time points (hours post inoculation) [33, 35, 36, 297]. The transcriptomics revealed that PAMP recognition induces suppression of a relatively large number of nuclear-encoded chloroplast-targeted protein genes (e.g., photosynthesis-related genes) at early time points (i.e., two, three and four hours post infection) [35, 36]. These data demonstrate that the chloroplast plays an early role in integrating pathogen and defense signals [35, 36].