Agriculture Reference
In-Depth Information
bition leads to accumulation of H
2
O
2
(Chen et al. 1995). Using the dimethyl urea
(a trap for H
2
O
2
), the effect of SA has been shown to be decreased suggesting that
SA acts through H
2
O
2
at least partly (Rao et al.
1997
). Though the production of
H
2
O
2
has been suggested to be crucial for the induction of disease resistance, yet
H
2
O
2
alone is insufficient to trigger PCD (Alvarez et al. 1998; Levine et al.
1994
;
Orozco-Ca'rdenas et al. 2001; Pellinen et al.
2002
). Application of exogenous SA
leads to increased cellular H
2
O
2
level in plant tissues when applied in suitable dose,
and has been found to induce HR signaling and SAR against pathogen (Lamb and
Dixon
1997
).
3.4 SA Regulated ROS Signaling, the Determinant of Defense
Metabolism and Tissue Fate
The role of ROS has also been explained in the regulation plant metabolism, there-
by in growth and development of the plant. ROS signals for gene expression (Desi-
kan et al.
2001
; Vanderauwera et al.
2005
) and to modulate activity of other crucial
signaling compounds, e.g. MAP kinase (Rentel et al.
2004
). Modification of protein
quaternary structure and activity of thiols in cellular pool has also been suggested
to have a widespread mechanism affecting the functional proteins regulated by cy-
toplasmic ROS level (Cooper et al.
2002
). Spatio-temporal distribution of ROS,
therefore, must be regulated sophistically (Mittler
2006
) at the boundary of com-
partmentalized gradients of organelles. The evolution of antioxidant system enables
plants to manage ROS toxicity within the limit to ensure their role as signal trans-
ducers (Mittler
2006
). Increased level of internal SA binds and inhibits the activity
of catalase (Chen et al. 1995) resulting in over-accumulation of H
2
O
2
. Continuous
and sustained accumulation of ROS in the absence of complementary activity of
antioxidant system donates free electrons to other electronegative groups second-
arily forming reactive nitrogen species and organic free radicals. This initiates an
oxidation chain reaction of membrane phospholipids disrupting homeostasis and
cellular integrity. The over-phosphorylated defense signaling and change in mem-
brane permeability and cellular pH commits this shift towards death signals. Reac-
tive nitrogen species react with ROS to form lethal peroxynitrile and nitrosonium
ions, adding further nitrosative stress (Zhao
2007
; del Río
2006
; Hayat et al.
2010
).
The determining step as to when and where a cell has to commit for cell death
is also regulated by the active participation of plant hormones. Once oxidative
stress crosses the threshold (a balance between oxidation and induced preventive
reduction to prevent minimal required setup for basal metabolic processes), the cell
switches over to PCD with simultaneous elicitation (HR) as defense mechanisms in
neighbourhood. Different combinations of hormones (SA, JA, NO) and secondary
signals (ROS, CaM, H
2
O
2
, Ca
2+
, kinases, lipid derivaties) have been found to be
involved in the initiation, propagation and containment phase of HR or PCD (Dangl
and Jones
2001
; Overmyer et al.
2003
). SA also mediates the lipid peroxidation,
