Modulation of chloroplast components and defense responses during programmed cell death in tobacco infected with Pseudomonas syringae

We examined how tobacco plants coordinate chloroplast components and defense responses during Pseudomonas syringae pv. tomato (Pst) infection. Tobacco leaves infiltrated with Pst induced weak necrosis at 24 h post-infiltration (hpi) and severe necrosis at 48 hpi. Membrane damage, as shown by cellular leakage and malondialdehyde, and H₂O₂ production began to increase at 12 hpi and continuously increased at 24–72 hpi in Pst-infiltrated leaves. Pst infection resulted in decreases in light-harvesting chlorophyll-binding proteins (Lhc), Lhcb transcripts, electron transport rate, and F_v/F_m, indicating the impairment in structure and function of photosystem II. Photochemical quenching, qP, continuously decreased in Pst-infiltrated leaves at 24–48 hpi, whereas nonphotochemical quenching, NPQ, exhibited a 2-fold increase at 24 hpi and a decrease at 48 dpi. In response to Pst infection, chlorophyll began to decrease at 48 hpi, whereas levels of protoporphyrin IX (Proto IX), Mg-Proto IX, Mg-Proto methylester, and protochlorophyllide drastically decreased or disappeared as early as 24 hpi. Pst-infiltrated leaves greatly up-regulated the expression of ROS scavenging genes, Fe-SOD, APX, and CAT1, as well as defense-related genes, PII, PR1, PR2, PALa, and CHS1. Our study suggests that the modulation of photosynthetic components during pathogen infection, particularly in relation to the fast degradation of photosensitizing porphyrin intermediates and the increase in photoprotective NPQ, may contribute to attenuating cellular damage in the early stages of programmed cell death induced by Pst.