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mutant plants is elevated after plastoquinone reduction. The RCD in the
lsd1
mutant plants
has been also proven to be inhibited by the mutation in
EIN2
, which encodes an ethylene
receptor. Additionally, the artificial impeding of foliar gas exchange in
lsd1
has been shown
to induce RCD, while high CO
2
level has prevented cell death in this mutant. Importantly,
lsd1
phenotype depends on EDS1 and PAD4, since in double mutants
eds1/lsd1
and
pad4/lsd1
PCD is inhibited [11,14,60]. The formation of ROS by plasma-membrane-bound NADPH ox‐
idase has been proposed to play a major role in RCD in the
lsd1
mutant during the shift from
short to long photoperiod, since the inhibition of this enzyme diminishes the formation of
lesions [61]. All these results suggest that LSD1 acts as a ROS rheostat and is necessary for
acclimation to conditions that promote oxidative stress. While LSD1 has been proven to neg‐
atively regulate the cell death, a highly similar protein - LOL1 (LSD1 like 1) is suggested to
be a positive PCD-regulator [62]. It has been proposed that LSD1 and LOL1 might function
in an antagonistic fashion to regulate the cell death propagation. Both LSD1 and LOL1 are
putative transcription factors (TF) or scaffold proteins since they possess zinc-finger do‐
mains responsible for DNA/protein binding. Such Zn-finger motif of the C2C2 class has
been found in plants, algae and protozoa, but not in animals. Apart from LSD1 and LOL1,
only five other
Arabidopsis
proteins contain one or more LSD1-like Zn-
fi
nger domains: LOL2,
LOL6 and already mentioned metacaspases: AtMC1, AtMC2 and AtMC3 [12]. The second
and third Zn-finger domains of LSD1 are responsible for interacting with metacaspase
AtMC1, which is a positive regulator of PCD. The
atmc1
mutation is able to suppress cell
death in
lsd1.
Furthermore, the interaction of LSD1 with AtbZIP10 transcription factor pre‐
vents its translocation to the nucleus. AtbZIP10 has been proven to be a positive mediator of
RCD observed in the
lsd1
mutant [63].
3. Reactive oxygen species in plants
The signaling during PCD proceeds mainly through the regulation of reactive oxygen spe‐
cies [60,64,65]. ROS are produced continuously as by-products of various pathways local‐
ized in chloroplasts, mitochondria and peroxisomes. They can occur as free radicals:
superoxide radical (O
2
•−
), hydroxyl radical (
•
OH), perhydroxyl radical (HO
2
•
), alkoxy radical
(RO
•
) or in non-radical forms: singlet oxygen (
1
O
2
) and hydrogen peroxide (H
2
O
2
). Most
abiotic stresses evoke the overproduction of ROS in plant tissues. Because of their high reac‐
tivity, ROS can cause damage of proteins, lipids, carbohydrates and nucleic acids, ultimately
leading to cell death (Figure 2).
The single reduction of O
2
results in the formation of O
2
•−
. From O
2
•−
other more reactive
ROS like
•
OH or HO
2
•
can be formed. The Haber-Weiss reaction generates hydroxyl radical
from hydrogen peroxide and superoxide. In this reaction O
2
•−
donates an electron to Fe
3+
, re‐
ducing ferric ion to ferrous:
Fe
3+
+ O
2
•−
→ Fe
2+
+ O
2
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