Agriculture Reference
In-Depth Information
The first step during the contact between a pathogen and its host is species specif-
ic in which elicitor binds to plasma membrane receptor for the process of elicitation
(Braun and Walker
1996
; Hanania and Avni
1997
), after that the genes of avirulence
brought by the pathogen (the elicitors) faces resistance from the host genes of resis-
tance. After proper recognition of the elicitors by the proper receptors of the plant,
defenses mechanism comes into play and they activate its genes of resistance (Hahn
1996
; Montesano et al.
2003
) through a series of complex reaction which is still un-
der investigation and might not be similar for all type of elicitors but it might give an
insight about their mechanism of action (Radman et al.
2003
, Namdeo
2007
). After
binding of the elicitor to plasma membrane a rapid ion fluxes across the membrane
occur (Mathieu et al.
1991
). As per other reports (Gelli et al.
1997
; Pitta-Alvarez
et al.
2000
; Mithöfer et al.
2001
) an influx of Ca
2
+
to the cytoplasm from the extra-
cellular environment and intracellular Ca
2
+
reservoir and stimulation of K
+
and Cl
−
efflux take place (Ivashikina et al.
2001
). It is followed by speedy changes in pro-
tein phosphorylation and protein kinase activation pattern upon elicitor treatment
(Yang et al.
1997
; Roemis
2001
); activation of protein kinases, in turn activate the
mitogen-activated protein kinase (MAPK), MAP-kinases and calcium-dependant
kinases catalyze mostly the Thr-Ser phosphorylation in the target proteins (Roemis
2001
). The MAP kinase cascade involves MAP kinase kinase kinase (MAPKKK)
proteins phosphorylating MAP kinase kinases that in turn phosphorylate MAP ki-
nases. Upon activation, MAPKs are transported to the nucleus where they phos-
phorylate specific transcription factors. Activation of G-protein by some workers
(Tyler
2002
; Luan
1998
; Roos et al.
1998
) suggested their involvement in the early
responses to elicitors (Legendre et al.
1992
), followed by the production of second-
ary messengers Ins (1, 4, 5)
P
3 and diacylglycerol (DAG) (Mahady et al.
1998
) me-
diating intracellular Ca
2
+
release, nitric oxide (Delledonne et al.
2002
; Huang et al.
2002
) and octadecanoid signalling pathway (Piel et al.
1997
). Later on AOS and cy-
tosol acidification is carried out by activation of NADPH oxidase (Leburun-Garcia
et al.
1999
) and reorganization of cytoskeleton take place (Kobayashi et al.
1995
)
and production of ROS like superoxide anion and H
2
O
2
(Low and Merida
1996
). It
is followed by accumulation of pathogenesis-related proteins (PR proteins) (Mittler
et al.
2004
). Earlier Bol et al. (
1990
) and Bowles (
1990
) reported individually about
the increase in PR proteins in response to elicitor. PR protein included chitinases,
glucanases, endoploygalactouranases that contribute to the release of signaling pec-
tic oligomers, hydroxyproline rich glycoproteins and protease inhibitors (Van Loon
and Van Strien
1999
). In hyper sensitive responses cell death occurs at the infection
site (Luan
1998
) and changes in the cell wall organization (lignification of the cell
wall, callus deposition) take place (Kauss et al
1989
). These all consequences are
responsible for the transcriptional activation of the corresponding defence response
genes (Memelnik et al.
2001
; Huang et al.
2002
) and accumulation of phytoalexins
and tannins (Pedras et al.
2002
) which stimulate the production of jasmonic and SA
as secondary messengers (Memelink et al.
2001
; Katz et al.
2002
) and plant cell
acquired systematic resistance (Lebrun-Garcia et al.
1999
). It is known that the se-
quence of these events and arrangements is a very complex process and is still under
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