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.