Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 211

and under different abiotic stresses. The loss of function in AtBI1 results in the mutant hy‐
persensitivity to environmental stimuli, whereas its overexpression in retarded PCD [37].
Numerous signals are constantly integrated by the cell to decide whether to enter or not the
cell death pathway. Different plant hormones are involved in the regulation of cell death un‐
der unfavorable conditions. One of the most important is SA which is intensively produced
in cells after pathogen infection or various abiotic stresses [38]. Many lesion mimic mutants
have constitutively elevated levels of SA [39]. At high concentrations, SA functions as a cell
death inducer in cooperation with other signals. It can be also transported beyond the site of
synthesis, acting as a signaling molecule and mediating systemic acquired resistance (SAR) -
a whole-plant resistance response that prepares plant for another infection [40]. The exis‐
tence of SA-dependent generation of ROS and the feedback control of SA synthesis by ROS
have been also demonstrated [41]. SA and ROS have been proposed to work in a potentia‐
tion feedback loop which acts to amplify signals leading to cell death. Another cell death
signaling molecule - nitric oxide (NO) has been also demonstrated to regulate key steps in
SA biosynthesis during pathogen infection [42]. Additionally, NO has been proven to coop‐
erate with ROS and SA in inducing cell death [43]. Other phytohormones regulating cell
death under stress conditions are JA, gibberellic acid (GA), abscisic acid (ABA) and ethylene
(ET). The latter is involved in the regulation of PCD during different developmental proc‐
esses and responses to environmental stimuli. ET has been proven to participate in the for‐
mation of aerenchyma in roots under hypoxia [14]. Antisense inactivation of the ET
biosynthetic enzyme - ACC oxidase delays leaf senescence and cell death in tomato [44].
Ethylene is also required for the continuation of ROS accumulation - external supply of ET
during cell death increases ROS production and causes accelerated spreading of cell death
[45]. JA is a plant signaling molecule best known for its role in the wound response but it is
also produced during wide range of biotic and abiotic stresses. It is involved in the inhibi‐
tion of ROS- and ET-dependent lesion propagation [46]. JA derivatives such as methyl jasm‐
onate (MeJA) are also engaged in the regulation of plant immune responses [47]. Upon
exposure to stress, MeJA is produced and causes the activation of PCD through the induc‐
tion of ROS generation, alterations in mitochondrial dynamics and photosynthetic collapse
[48]. Another phytohormone - GA has been proven to promote cell death in cooperation
with ROS, whereas ABA delays GA-induced PCD. Such counteracting role of these hor‐
mones relates to their influence on the ROS-scavenging enzymes expression [49]. ABA has
been also shown to delay ET- and GA-induced cell death in rice epidermal cells [50]. All
these interactions between phytohormones and ROS indicate the complexity of PCD regula‐
tion. Overmyer and colleagues [39] suggested the following series of events during oxida‐
tive stress-triggered PCD. At the site of lesion initiation, the action of ROS is amplified.
Increased ROS accumulation together with SA induces the cell death. During the initial
process, JA signaling is hindered by SA and ET. Meanwhile, the burst of ET from the initial
site disperses to surrounding cells, amplifies ROS production that promotes the lesion
spread. This is the signal to induce competitive reactions to PCD. Cell death results in the
production of JA which acts as a negative regulator of the oxidative cell death cycle. JA,
through the suppression of SA biosynthesis/signaling and the attenuation of ET sensitivity,
inhibits the lesion propagation.