Agriculture Reference
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programmed cell death is affected by light. The spread of wound-induced PCD in maize tis‐
sue has been shown to be transmitted by chloroplast-produced ROS [134]. It has also been
found that the HR-mediated cell death is accelerated by the loss of chloroplast function
[154]. Moreover, a study using light- and dark-grown plant cell culture has proven that they
respond differently to PCD-inducing stimuli, resulting in various levels of DNA fragmenta‐
tion and cell-content condensation [65]. Direct induction of programmed cell death by expo‐
sure of
Arabidopsis
rosettes to excess light (EL) (2000 μmol of photons m¯² s¯¹) has also been
demonstrated [130].
Although ROS produced during the progress of PCD are damaging for the cell, they are also
needed as messenger molecules preparing other cells for a struggle with stress conditions.
H
2
O
2
is thought to freely diffuse across biological membranes, thus it has been proposed to
directly influence the function of extra-chloroplastic signaling components. The possibility
that H
2
O
2
acts as an intracellular messenger molecule has been suggested since it triggeres
systemic response to EL [130]. When low-light-grown
Arabidopsis
rosettes have been partial‐
ly exposed to EL, unexposed leaves have become acclimated to EEE and to photooxidative
stress. This phenomenon, termed systemic acquired acclimation (SAA) is attributed to chlor‐
oplasts, as it is associated with specific changes in redox status of the photosynthetic elec‐
tron carrier chain. Such redox changes lead to the alternation in transcription profiles,
triggering SAA. By the use of photosynthesis inhibitors: 3,4-dichlorophenyl-1,1-dimethylur‐
ea (DCMU), which blocks the reduction of PQ and 2,5-dibromo-3-methyl-6-isopropyl-
p
-ben‐
zoquinone (DBMIB), that blocks PQ oxidation, it has been demonstrated that the PQ pool
redox status is predominantly responsible for SAA [60,130]. DCMU has been also proven to
inhibit effects of EEE, such as higher NPQ, production of ET, H
2
O
2
and decrease in stomatal
conductance. On the other hand, DBMIB has been shown to trigger the production of ET,
H
2
O
2
and stomatal closure even under low light. These results indicate that the redox status
of PQ pool and NPQ play a critical role in the initiation of response to EEE, in ET and H
2
O
2
signaling and consequently in the PCD regulation [11,60,130,155,156]. Activation of the SA-
dependent pathway in response to EEE has been also observed after an initial induction of
ROS/ET signaling [60]. Other hormones such as JA and ABA, synthesized at least partially
within the chloroplast, also participate in response to EEE [149]. A large number of tran‐
scripts encoding different antioxidant defense enzymes is induced in local and systemic
leaves after EL treatment. Apart from APX1 and APX2 [130], higher expression level has
been proven for GPX2, GSTs, APX3 and CSD1 [60,157]. Furthermore, a recent study has sug‐
gested that local and systemic responses to EL are associated with changes in the plasma
membrane electrical potential (photoelectrophysiological signaling - PEPS). During the EL
incident, PEPS has been shown to be initiated by quantum redox changes in PSII, trans‐
duced by bundle sheath cells and its systemic propagation has been proven to be dependent
on APX2 function. Therefore, PEPS is suggested as a new component of signaling cascades
that regulate light acclimatory responses. Furthermore, it has been proposed that leaves are
able to memorize different EL episodes and use this information for improving their accli‐
mation and survival under prolonged periods of unfavorable light conditions [131].
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