development depend on the efficacy of rhizobial strains [33]. Significantly
increased levels O • À
2
and Н 2 О 2 were found in the pea roots after inoculation by
incompatible strains of bacteria R. leguminosarum bv. phaseoli [33]. This may
indicate ROS involvement in protection against infection of the pea roots with
incompatible rhizobia. The inoculation of pea roots by compatible
R. leguminosarum bv. viciae strains also increased O • À
2
and Н 2 О 2 levels with
simultaneous stimulation of antioxidant enzymes in pea seedling epicotyls. The
latter suggests that the plants have certain mechanisms to prevent bacterial infection
in organs that cannot form nodules [33]. It is supposed that limitation of rhizobial
infection is connected with triggering a reaction similar to the systemic acquired
resistance in phytopathogenesis [34] or systemic induced resistance as in the case of
infection by nonpathogenic microorganisms [33]. ROS can upregulate expression
of genes encoding hydrolytic enzymes, stress-protective proteins, enzymes
involved in synthesis of phenolic compounds, phytotoxins, and other substances
required for development of acquired resistance to pathogens [124]. Thus, ROS
generation is among key components of the plant response to infection with both
compatible and incompatible bacteria.
The elevated levels of ROS were found to be necessary for the effective penetration of bacteria into plant tissues, since the decrease of ROS and
•
NO levels
prevented formation of bacterial infection thread and delayed nodule formation
[34, 46]. Mutant strain of S. meliloti, which degrades H 2 O 2 very efficiently (owing
to the overexpression of a catalase gene), demonstrated altered infection properties
and induced the formation of a reduced number of nodules on roots of symbiotic
plant Medicago [94]. H 2 O 2 was found to be necessary for the optimal propagation of
infectious bacterial threads inside root hairs and membranes of plant cells
[41]. In addition, ROS and
•
NO were found to be involved in the induction of
early nodulin gene expression and the repression of plant defense, thereby favoring
the establishment of the symbiosis [44–46, 93]. Moreover, H 2 O 2 appears to control
a key step of the interaction, since H 2 O 2 is relatively long-living ROS and can easily
diffuse via biological membranes and act at distant places. An S. meliloti strain,
overexpressing a catalase gene, showed a delayed nodulation phenotype associated
with aberrant infection threads [41].
At the initial stages of symbiosis, an oxidative burst occurs in the place
of bacterial infection [38]. Oxidative burst can have a dual function in legumerhizobium symbiosis. First, temporal oxidative burst inhibits the protective reactions
of plants on penetration of compatible bacteria. On the other hand, intense oxidative
burst can activate protective mechanisms of plants under incompatible conditions for
symbiosis [125]. During the infection process, production of O • À
2
and H 2 O 2 was
localized in infection threads and infected cells [38]. In P. vulgaris, a transient
increase of ROS was detected at the tip of root hairs within seconds after addition
of Nod factors [35]. However, after several minutes H 2 O 2 production appears to be
inhibited by Nod factors [32]. It was suggested that ROS production is necessary
for infection initiation, but prolonged and elevated levels are detrimental to nodulation [46]. Bacterial Nod factors were found to stimulate oxidative burst by blocking
306
U. Y. Stambulska and M. M. Bayliak
increased levels O • À
2
and Н 2 О 2 were found in the pea roots after inoculation by
incompatible strains of bacteria R. leguminosarum bv. phaseoli [33]. This may
indicate ROS involvement in protection against infection of the pea roots with
incompatible rhizobia. The inoculation of pea roots by compatible
R. leguminosarum bv. viciae strains also increased O • À
2
and Н 2 О 2 levels with
simultaneous stimulation of antioxidant enzymes in pea seedling epicotyls. The
latter suggests that the plants have certain mechanisms to prevent bacterial infection
in organs that cannot form nodules [33]. It is supposed that limitation of rhizobial
infection is connected with triggering a reaction similar to the systemic acquired
resistance in phytopathogenesis [34] or systemic induced resistance as in the case of
infection by nonpathogenic microorganisms [33]. ROS can upregulate expression
of genes encoding hydrolytic enzymes, stress-protective proteins, enzymes
involved in synthesis of phenolic compounds, phytotoxins, and other substances
required for development of acquired resistance to pathogens [124]. Thus, ROS
generation is among key components of the plant response to infection with both
compatible and incompatible bacteria.
The elevated levels of ROS were found to be necessary for the effective penetration of bacteria into plant tissues, since the decrease of ROS and
•
NO levels
prevented formation of bacterial infection thread and delayed nodule formation
[34, 46]. Mutant strain of S. meliloti, which degrades H 2 O 2 very efficiently (owing
to the overexpression of a catalase gene), demonstrated altered infection properties
and induced the formation of a reduced number of nodules on roots of symbiotic
plant Medicago [94]. H 2 O 2 was found to be necessary for the optimal propagation of
infectious bacterial threads inside root hairs and membranes of plant cells
[41]. In addition, ROS and
•
NO were found to be involved in the induction of
early nodulin gene expression and the repression of plant defense, thereby favoring
the establishment of the symbiosis [44–46, 93]. Moreover, H 2 O 2 appears to control
a key step of the interaction, since H 2 O 2 is relatively long-living ROS and can easily
diffuse via biological membranes and act at distant places. An S. meliloti strain,
overexpressing a catalase gene, showed a delayed nodulation phenotype associated
with aberrant infection threads [41].
At the initial stages of symbiosis, an oxidative burst occurs in the place
of bacterial infection [38]. Oxidative burst can have a dual function in legumerhizobium symbiosis. First, temporal oxidative burst inhibits the protective reactions
of plants on penetration of compatible bacteria. On the other hand, intense oxidative
burst can activate protective mechanisms of plants under incompatible conditions for
symbiosis [125]. During the infection process, production of O • À
2
and H 2 O 2 was
localized in infection threads and infected cells [38]. In P. vulgaris, a transient
increase of ROS was detected at the tip of root hairs within seconds after addition
of Nod factors [35]. However, after several minutes H 2 O 2 production appears to be
inhibited by Nod factors [32]. It was suggested that ROS production is necessary
for infection initiation, but prolonged and elevated levels are detrimental to nodulation [46]. Bacterial Nod factors were found to stimulate oxidative burst by blocking
306
U. Y. Stambulska and M. M. Bayliak