Chemistry Reference
In-Depth Information
Recently, Kadono et al. (
2010
) have demonstrated that O
3
challenge induces the
activation of PM anion channel which is an early prerequisite of the O
3
-induced
cell death in A. thaliana. As the additions of ROS scavengers or iron/copper
chelators to the cells of A. thaliana effectively lowered the level of cell death
induced by O
3
(Kadono et al.
2010
), the central roles for ROS members, chiefly
1
O
2
and H
2
O
2
(and derived HO
•
), in O
3
-induced acute damages observed in the
earlier study using tobacco cells was further confirmed (Kadono et al.
2006
). In
A. thaliana, the obtained data further suggested the interplay between anion
channel activation, Ca
2+
influx and ROS generation by RBOHs in mediating the
oxidative cell death (Kadono et al.
2010
). This interplay might be fuelled by
several ways in addition to direct ROS generation by O
3
, namely, increase in anion
channel activity by oxalate generated via ascorbate degradation by O
3
(Tran et al.
2013
), and H
2
O
2
generation by SA and ABA.
Since NO and plant hormones SA, JA, ABA and ET are involved in deter-
mining the duration and extent of O
3
-induced cell death propagation (Baier et al.
2005
; Kangasjärvi et al.
2005
; Tamaoki
2008
; Ahlfors et al.
2009
), their impact in
the newly proposed model was further examined (Kadono et al.
2010
). Mutant
lines and pharmacological analysis indicated that JA, ET and NO are not the major
factors in the signalling pathways leading to cell death in Arabidopsis cultured
cells. On the contrary, ABA synthesis would take place in response to O
3
since
pre-treatment on cells with fluridon was able to counteract the O
3
effect.
In the same manner, involvement of SA in O
3
-induced cell death was assessed
using the suspension-cultured cells derived from NahG, cpr5 and npr1 plants, which
are impaired in SA signalling, and sid2 mutant, which are impaired in SA biosyn-
thesis through the isochorismate pathway (Fig.
1
). The extent of O
3
-induced cell
death in NahG, cpr5 and npr1 cell lines showed significant decreases, revealing that
O
3
-induced death depends on SA signalling in Arabidopsis cells. Interestingly, Sid2
cell line presented the same extent of cell death compared to the level recorded for
O
3
treatment in wild type cells (col), suggesting that SA synthesis is not required for
this acute cell death induction in model cells. If this is the case, how the SA sig-
nalling pathway could be activated? As SA could be rapidly released in the apoplast
from the storage form of SA, salicylic acid b-glucoside (SAG) (Hennig et al.
1993
;
Kawano et al.
2004b
), SAG pool may be serving as the source of O
3
-dependently
acting SA. This view must be testified in the future studies.
As the possible involvement of SA in O
3
action was suggested, we have also
tested the putative impact of SA on anion channel activation. As shown in Fig.
2
,SA
at 200 lM, a physiological concentration, induced a rapid but slight hyperpolari-
sation of the cells followed by a larger depolarisation event within a few minutes.
The temporal changes in the PM potential following addition of SA was compared
with changes in anion channel activity. As the delayed depolarization being corre-
lated with an increase in anion channel activity, SA could not be responsible for the
early depolarization induced by O
3
but SA could also fuel the generation of H
2
O
2
and Ca
2+
influx involved in O
3
-induced cell death. The SA-induced generation of
H
2
O
2
via stimulation of peroxidise and/or NADPH-oxidase is known to lead to Ca
2+
influx (Kawano and Muto
2000
; Kawano et al.
2004a
,
b
,
c
) which could explain the
Search WWH ::
Custom Search