Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 212

During early events of hypersensitive response, ion fluxes are induced. Ca 2+ influx caused
by external hydrogen peroxide application has been demonstrated to be sufficient in trigger‐
ing HR in soybean cells [51]. Moreover, several cell death signaling proteins in plants exhibit
a function associated with lipids. Two Arabidopsis mutants, eds1 and pad4 have been proven
to be defective in HR signaling. EDS1 ( ENHANCED DISEASE SUSCEPTIBILITY 1 ) and
PAD4 ( PHYTOALEXIN DEFICIENT 4 ) genes encode proteins with triacylglycerol lipase
function [52,53] which provides a genetic evidence that phospholipid signaling is involved
in the induction of PCD. The level of phosphatidic acid (PA), produced by the phospholi‐
pase D (PLD) increases during defense response [54]. One of PLD isoforms in Arabidopsis
has been shown to impair ROS-mediated PCD in response to biotic and abiotic stimuli [55],
indicating the role of PA as a negative signal of cell death propagation. It is also hypothe‐
sized that the perturbation in sphingosine transport may cause cell death in plants since the
mutation in ACD11 gene encoding a sphingosine-transport protein, results in a lesion-mimic
phenotype that is dependent on EDS1, PAD4, SA and light [56]. EDS1 and PAD4 are exten‐
sively studied regulators of PCD. They constitute a regulatory hub that transduces redox
signals in response to biotic and abiotic stresses. Both EDS1 and PAD4 are also important
activators of SA signaling and mediate antagonism between JA and ET pathways during de‐
fense responses [57]. Furthermore, they are responsible for the biotic and abiotic stress-in‐
duced PCD in the LESION SIMULATING DISEASE 1 ( LSD1 ) mutant [58,59]. The lsd1
mutant fails to limit the spread of PCD under long photoperiod or after the infection with
avirulent pathogens. It is one of the best characterized mutants in terms of programmed cell
death. The lsd1 mutant exhibits a runaway cell death (RCD) phenotype (Figure 1B) manifest‐
ed in the inability to restrict the progression of cell death once it has been initiated [9,11],
which provides a genetic evidence for LSD1 as a PCD repressor.
Figure 1. Runaway cell death (RCD) phenotype in the lsd1 mutant. 3-week-old Arabidopsis thaliana rosettes grown in
long photoperiod (>11 h); A - wild type; B - lsd1 mutant. Arrows indicate leaves undergoing runaway cell death.
The lsd1/cao double mutant which has reduced photosystem II (PSII) antenna size and thus
reduced light absorption capacity due to the cao mutation in chloroplast signal recognition
particle (cpSRP43), exhibits higher non-photochemical quenching (see later) and inhibited
RCD after excess light exposure in comparison to the lsd1 mutant. Therefore, the RCD in the
lsd1 mutant has been linked to the amount of light energy absorbed in excess by the PSII
light harvesting complex [11]. It has been shown that ET and ROS production in the lsd1