Abstract: Pseudomonas syringae pv. tabaci (Pst) is a hemi-biotrophic bacterial pathogen that causes the formation of brown spots named wildfire disease. Pst has received considerable attention in recent years. However, most of the studies focused on the tolerance and defense mechanisms of the host and non-host plants against Pst infection and a toxin originally described as being from Pst named tabtoxin, little information is available on the photosynthetic performance of tobacco leaves after Pst infection. Exploring the effects of Pst on the photosystem Ⅱ (PSⅡ) will not only help in clarifying tobacco-Pst interaction mechanisms, but also deepen the understanding of bacterial pathogen disease from a physiological perspective. By analyzing chlorophyll a fluorescence transient, performing western blot of thylakoid membrane and measuring the content of reactive oxygen species (ROS) and total chlorophyll, the effects of Pst on PSⅡ in tobacco were studied under light (200 μmol·m^-2·s^-1) or dark conditions. The results showed that chlorophyll content significantly decreased and significant chlorosis of the infiltrated zone was observed compared to the untreated ones, and tobacco leaves exhibited a visible and overt wildfire symptom at 3 days post Pst infection (dpi) under light and dark conditions. The H₂O₂ content increased at 3 dpi compared to untreated ones in tobacco leaves under light and dark conditions, and was much higher under light than dark condition. Besides, markedly increase of the normalized relative variable fluorescence at the K step (W_K) and the relative variable fluorescence at the J step (V_J), significant decrease of maximal quantum yield of PSⅡ (F_v/F_m) and density of Q_A^- reducing PSⅡ reaction centers per cross section (RC/CSm) were observed in tobacco leaves after Pst infection at 3 dpi under light and dark conditions. Moreover, inhibition of the K and J steps was more pronounced in the dark, as indicated by the greater increase of W_K and V_J under darkness compared with the light conditions during Pst inoculation. Dramatic (net) degradation of D1 protein and PsaO, the core protein of PSⅡ reaction center and oxygen evolving complex (OEC) respectively, at 3 dpi after Pst infection was observed in tobacco leaves under both light or dark conditions, and the decline was more exacerbated under dark than light condition. The results indicated that the electron transport from Q_A to Q_B of photosynthesis electron transport chain was severely blocked, OEC was damaged on both the donor and acceptor sides, and the reaction center of PSⅡ was severely damaged by Pst infection in tobacco lea-ves under either light or dark condition. Photoinhibition and photoinhibition-like damage of PSⅡ was observed after Pst infection, and the damage to PSⅡ under dark condition was much more severe than under light condition in tobacco leaves.