© Benaki Phytopathological Institute
Sakr
6
solani)
by 34.2% in rice plants (Schurt
et al.,
2014).
For air- and soil-borne fungi, the mode
of silicon action in a number of components
of host plant resistance could be summa-
rized as follows (Datnoff
et al.,
2007; Datnoff
and Heckman, 2014): silicon delays the incu-
bation and latent periods, decreases conidi-
al production, and reduces some features of
the lesions produced by the fungal patho-
gens (expansion rate, size and number).
Subsequently, disease development and/or
definitive disease incidence is dramatically
decreased, and the resistance of susceptible
cultivars is, in some cases, raised to nearly
the same level as that of cultivars with com-
plete or partial resistance. Moreover, for sus-
ceptible and partially resistant rice cultivars,
the observed disease resistance is greatest
when silicon is applied to the soil and is root-
absorbed as oppose to when it is applied
to the foliage (Rezende
et al.,
2009). This is
mainly due to the silicon transporters which
are not expressed in the leaves. Regarding
foliar sprays, the disease suppressive effects
observed are probably due to silicon being
deposited on the leaf surface and thus, hav-
ing an osmotic or pH effect. However, the
underlying mechanisms that govern disease
protection when silicon is root-absorbed re-
main largely unclear (Datnoff
et al.,
2007;
Datnoff and Heckman, 2014).
4. Mechanisms of silicon-enhanced
resistance
In spite of the many scientific reports about
silicon effects on fungal pathogens, the
properties, spectrum of efficacy and mode
of action of silicon remain largely specula-
tive (Ghanmi
et al.,
2004; Fauteux
et al.,
2005;
Datnoff
et al.,
2007; Van Bockhaven
et al.,
2013). Under controlled hydroponic condi-
tions, silicon does not affect plant growth or
development (Ma and Yamaji, 2006). How-
ever, where plants are exposed to multiple
stresses, silicon plays an important role in
plant health (Epstein, 2009). Generally, the
effect of silicon on resistance of plants to
diseases is considered to be due to either an
accumulation of absorbed silicon in the epi-
dermal tissue, or an expression of metabolic
or pathogenesis-mediated host defense re-
sponses (Fauteux
et al.,
2005; Datnoff
et al.,
2007; Van Bockhaven
et al.,
2013).
4.1. Physical defense
For the first hypothesis of silicon physi-
cal enhanced resistance, silicon deposited
on the tissue surface acts as a physical barri-
er that protects plants from fungal infection.
In this model, the increase of resistance has
been associated with several factors, such as
(1) the density of the long and short silicified
cells present in the epidermis of the leaves,
(2) the thick silica layer below the cuticle, (3)
the double cuticular layer, (4) the thickened
silicon-cellulose membrane, and (5) the pa-
pilla formation (Fauteux
et al.,
2005; Datnoff
et al.,
2007; Van Bockhaven
et al.,
2013).
Silicon prevents physical penetration by
pathogenic fungi, strengthens plants me-
chanically, and / or makes the plant cell less
susceptibletoenzymaticdegradationbyfun-
gal pathogens. Yoshida
et al.
(1962) reported
that a thick layer of silica is formed beneath
the cuticle of rice leaves and sheaths after
polymerization of monosilicic acid. This sil-
icon layer beneath the cuticle might be par-
tially responsible for impeding pathogen
penetration. Furthermore, silicon might also
form complexes with organic compounds in
the wall of the epidermal cells, thus increas-
ing their resistance to degradation by en-
zymes released by plant pathogenic fungi
(Volk
et al.,
1958). It was also suggested that
silicon may be associated with lignin-carbo-
hydrate complexes present in the cell wall of
epidermal cells (Inanaga
et al
.
,
1995).
Regarding cytological and pathogen-
ic features associated with physical resis-
tance, silicon deposited on the tissue sur-
face decreases the number of lesions on
leaf blades, or increases the incubation pe-
riod, as reported for the
Pyricularia grisea
–
and
Rhizoctonia solani
–rice pathosystems
(Rodrigues
et al.,
2001; Seebold
et al.,
2004).
Moreover, Kim
et al.
(2002) reported that si-
licified epidermal cell walls were closely as-
