Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 228

nents, from which expansins are key proteins engaged in this process. The onset of cell
expansion involves pumping of protons into the cell wall, which makes the surrounding
more acidic. As a result, expansins become activated. They loosen connections between cel‐
lulose microfibrils, which leads to the cell wall relaxation, water uptake and consequently
the cell expansion [182]. It has been demonstrated that the mild osmotic stress causes the in‐
duction of expansin genes [183].
Photosynthesis is one of major processes affected by water deficit since stomata closure
causes reduced CO 2 diffusion to the chloroplast. As a result of the inhibition of photosynthe‐
sis and the predominance of photorespiration, ROS are generated [184]. It has been demon‐
strated that in drought-stressed plants, the ABA-controlled stomata closure is mediated by
H 2 O 2 [185]. Under severe drought stress, some antioxidant enzymes have been shown to be
highly induced [186]. However, studies on many drought-stressed crop species showed an
inconsistency in their expression since in some cases they have been induced, but in other
repressed, suggesting that different ROS balance may be required during different response
phases [187].
During water deficit, ROS are responsible for the induction of leaf senescence, which is exe‐
cuted through the programmed cell death and plays an important role in the plant survival.
It contributes to the nutrients remobilisation during stress and allows the rest of plant to
benefit from them and stay alive. Drought-induced PCD enables also the abscission of some
leaves and thus the avoidance of further water loss through the transpiration. It occurs grad‐
ually and is manifested by specific biochemical and molecular changes such as chromatin
condensation, thylakoid swelling, lipid peroxidation, degradation of chlorophyll (leaf yel‐
lowing) and proteins. Apart from ROS, cytokinins and ABA have been shown to be in‐
volved in the regulation of water-deficit-triggered senescence [123]. Recent studies have
shown that the water deficit triggers PCD not only in green tissues but also in plant root
tips. Apical meristem cells of primary roots undergoing PCD, demonstrate increased size of
vacuole, degradation of organelles and the collapse of plasma membrane [188].
Early events in the perception of drought stress signals include the activation of transcrip‐
tion factors belonging to such classes as DREB/CBF (e.g. DREB1a, DREB2a), ABF (e.g. ABF2,
ABF4), MYB (e.g. MYB2), MYC, NAC and WRKY. Many of them possess stress responsive
cis-regulatory elements in their promoter sequences like abscisic acid-responsive elements
(ABRE) and drought-responsive elements (DRE) [189-191]. The plasma membrane-associat‐
ed NTL4 (NAC transcription factor) after drought or ABA treatment has been shown to be
proteolytically activated and transported to the nucleus where it induces expression of
NADPH oxidase involved in ROS generation [192]. Moreover, the dehydration stimulates
expression of BAX inhibitor-1 (AtBI-1). The atbi1 mutant has been shown to display more
severe cell death, indicating that ER-located AtBI-1 modulates the water-deficit-induced
PCD [188]. Drought stress has been also proven to regulate the expression and activity of
aquaporins - a family of channel proteins that facilitate the transport of water along trans‐
membrane water potential gradients [193].
Upon soil water deficit, the accumulation of ABA and the induction of ABA-associated sig‐
naling genes occur. ABA induces various second messengers such as cytosolic Ca 2+ , ROS