Impact of Salicylic Acid on the Transport and Distribution of Sugars in Plants - Salicylic Acid: Plant Growth and Development - page 94

even in the presence of SA. The mpk 4 mutant accumulating much SA concentra-
tions is characterized by the accumulation of AtGSL5 transcript (Petersen et al.
2000 ). In this case, activity of ß-1,3-glucan synthase was increased and callose was
accumulated (Østergaard et al. 2002 ). When the mpk 4 mutant contained the bac-
terial gene NahG preventing SA accumulation, expression of AtGSL5 gene was
suppressed. This argues for SA requirement for GSL5 gene functioning.
The content of a protein degrading callose, ß-1,3-glucanase, depends on SA as
well. In our experiments, tobacco leaf treatment with SA (3-20 h) resulted in the
suppression of ß-1,3-glucanase activity (Serova et al. 2006 ). Such suppression was
correlated with callose accumulation. However, ß-1,3-glucanase not only degrades
callose and in such a way is involved in the control of plasmodesma permeability,
it is one of the main defensive proteins. May be therefore, at longer SA treatment,
the synthesis of this enzymes was induced simultaneously with the development of
defensive processes (Shah and Klessig 1996 ; Kang et al. 1998 ; Zhen and Li 2004 ).
Callose deposition around the plasmodesma is an important element of defense
against the pathogen. However, callose deposition around the site of infection is
not a universal way of plant defense. Thus, at fungal infection, callose synthesized
by the plant supplies to the fungus an additional nutrition, stimulating its growth
(Jacobs et al. 2003 ). After identification in Arabidopsis thaliana glucan synthase-
like gene AtGSL5 (Østergaard et al. 2002 ), plants with silenced callose synthase
gene GSL5 (Jacobs et al. 2003 ) were produced. In such plants, wound callose and
callose forming papilles at infection with powdery mildew and other fungal
pathogens were absent. In spite of the absence of callose, plant resistance did not
reduce and papilles were formed but using other compounds. Similar data were
obtained on the arabidopsis pmr4 mutant, which did not synthesize callose at
infection with powdery mildew; such plants were even more resistant than wild-
type plants. It turned out that the cause for improved resistance in plants deficient
in callose was the activation of SA-depending responses (Nishimura et al. 2003 ).
The authors concluded that callose formation was on the one hand a rapid plant
response to fungal infection and on the other hand results finally in the inhibition
of SA-dependent defense responses.
Cytoplasmic calcium. The callose content depends on cytoplasmic calcium
which is essential for the synthesis of callose, most likely due to its direct effect on
the Ca-sensitive callose synthase (Köhle et al. 1985 ; Kauss 1985 ). In the presence
of chelator (EDTA), the deposition of callose is sharply reduced (Eschrich 1965 ;
Köhle et al. 1985 ). The inhibitors of Ca 2+ -channels, nifedipin and gadolinium, also
block the synthesis of callose (Kartusch 2003 ). Stress exposure, induces the entry
of calcium into cells that causes an increase in its concentration near membrane,
activating callose synthesis (Bhuja et al. 2004 ). SA can act similarly.
Cytoskeleton. The actomyosin complex may be involved in the regulation of
intercellular transport through plasmodesmata. Both actin and myosin were im-
munolocalized to these transcellular channels (Blackman and Overall 1998 ; Radford
et al. 1998 ; Aaziz et al. 2001 ; Baluška et al. 1999 , 2001 , 2004 ). The inhibitors of
actin cytoskeleton, cytochalasin and latrunculin B were interrupted with callose