Figure Legends
Fig. 1 Preferential impairment of OEC induced by light. (A) Variations in the amplitude L 1 of the kinetics component calculated by fitting the DF decay kinetics to the time function DF(t ) = L 1 × exp(-t/τ 1) + L 2 × exp(-t/τ 2) + L 3. The inset shows DF decay kinetics at I 1 in response to light exposure. (B) Changes in the relative variable fluorescence at the K-step (W k) in response to light exposure. (C) Variations in OEC peripheral proteins PsbO, PsbP and PsbQ during light exposure. Values were % of dark 100% and normalized to RbcL amount. The significantly different value (Tukey’s tests, P < 0.05) from 0 min or dark is marked with an asterisk (*). (D) Changes in the normalized chlorophyll fluorescence intensity of OJIP transients (F t/F O) in response to light exposure and plotted on a logarithmic time scale. (E and F) Photoinhibition measured by the decrease inF v/F m in the presence of lincomycin. (E) The decreases ofF v/F m standardized based on 0 min fitted well with the functionF v/F m = exp (-KPI × t) (all R 2 values > 0.9). (F) Dependence of the KPI on photon flux density (P < 0.05). The means ± s.d. were calculated from three independent samples. The means ± s.d. were calculated from three independent samples. Each curve represents the average of three replicates.
Fig. 2 GO enrichment analysis and PPI network of DEPs. (A) The biological processes in GO enrichment analysis of DEPs. The DEPs are on the left and the GO pathway names are on the right (P < 0.05). (B) PPI network of DEPs. Red nodes indicate upregulated proteins and blue nodes indicate downregulated proteins. The larger size of the node represented the higher connectivity of the protein, which indicated more interactions with other proteins. The width of the line represents the capacity of the interaction between proteins.
Fig. 3 Photosynthetic activity and NPQ response to light exposure. (A) Changes in O2 evolution rate and Rubisco carboxylase activity in response to light exposure. The significantly different value (Tukey’s tests, P < 0.05) from 0 min is marked with an asterisk (*). (B) chlorophyll fluorescence during NPQ formation. (C) The kinetics of NPQ induction fitted with the function NPQ = A × exp (-x/t ) + y0. The means ± s.d. were calculated from three independent samples.
Fig. 4 The relevant parameters of PSII damage response to light exposure. (A) Variations in probabilities for an electron moving further than QA(1-V J) and chloroplast1O2 contents after light exposure. The significantly different value from Dark (Tukey’s tests, P< 0.05) is marked with an asterisk (*). (B) Changes in OJIP transients in response to light exposure and plotted on a logarithmic time scale. The means ± s.d. were calculated from three independent samples. Each curve represents the average of three replicates.
Fig. 5 AsA and PSII-CEF response to light exposure.(A) Variations in GLDH contents determined by densitometry and chloroplast AsA levels in response to light exposure. The significantly different value from 0 min (Tukey’s tests, P < 0.05) is marked with an asterisk (*). (B) Changes in chlorophyll a fluorescence kinetics as summarized by ΔV t and OJIP curves in response to light exposure and different concentrations of DMBQ. The signals are plotted on a logarithmic time scale. Each curve represents the average of three replicates.
Fig. 6 Photoprotection of AsA and PSII-CEF response to light exposure. (A) Time course of the changes in maximal photochemical yield of the PSII (F v/F m) and the relative variable fluorescence at the K-step (W k) in response to different inhibitors. The significant effects of rotenone and DMBQ onF v/F m andW K during HL exposure were examined with repeated measures ANOVA (all p values < 0.05). (B) The changes in PSII RC proteins D1, CP43 and OEC peripheral proteins PsbO, PsbP, PsbQ after 3 h of treatment. Values were % of dark 100% and normalized to RbcL amount. The significantly different value from 0 min (Tukey’s tests, P < 0.05) is marked with an asterisk (*). Data are expressed as mean ± s.d. (n = 3).
Fig. 7 Schematic model of donor-side photoinhibion derived from the photoinactivated OEC. The red arrows represent the activated pathways in which the degree of activation are represented by the width of line and the dark arrows represent the pathways that were not significantly activated. Positions of photosynthetic complexes in thylakoid membrane are based on published annotations (Eberhard and Finazzi GWollman, 2008; Gururani et al., 2015; Li et al., 2018). PQ, plastoquinone; Cytb6f, cytochrome b6f; PC, plastocyanin; Fd, ferredoxin; FNR, ferredoxin NADP+ reductase; MDA, monodehydroascorbate; Mal, malate; PTOX, ubiquinol oxidase; GLYK, D-glycerate 3-kinase; MDH, malate dehydrogenase; OAA, oxaloacetic acid; SOD, superoxide dismutase; APX, ascorbate peroxidase.