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| Authors: | H. Otani, M. Kodama, K. Kohmoto |
| Keywords: | Alternaria alternata Japanese pear pathotype, AK-toxin, elicitor, defense reaction, plasma membranes, accessibility |
Abstract:
Alternaria alternata Japanese pear pathotype causes black spot of Japanese pear (Pyrus pyrifolia). Infection behavior of the pathogen was equal on leaf surface of susceptible and resistant cultivars, but penetration was detected only in susceptible leaves.
The pathogen released a host-specific toxin (AK-toxin) immediately after spore germination which is toxic to susceptible cultivars but harmless to resistant ones.
Avirulent spores of A. alternata did not produce AK-toxin and could not penetrate.
When the avirulent spores were inoculated together with AK-toxin, the fungus could invade susceptible pear tissues.
Conversely, inhibition of AK-toxin production in germinating spores of the pathogen markedly decreased the infection. A. alternata, regardless of their pathogenicity, released a factor (elicitor) which induces defense reaction against fungal invasion in pear leaves from germinating spores.
Activity of the elicitor was suppressed completely in susceptible leaves when the elicitor was added with AK-toxin, and avirulent spores could invade susceptible pear tissues.
The primary effect of AK-toxin was on the plasma membranes of susceptible pear cells and AK-toxin had pleiotropic effects on susceptible cells after specific recognition on plasma membranes.
The protection of plasma membrane dysfunction which was induced by AK-toxin led to the suppression of fungal invasion.
However, even if the process of host cell death after plasma membrane dysfunction was blocked, fungal invasion was easily established.
Based on these results, infection mechanism of the pathogen in susceptible Japanese pear is summarized as follows: (i) release of AK-toxin and elicitor from germinating spores before penetration; (ii) specific recognition of AK-toxin on plasma membranes; (iii) induction of plasma membrane dysfunction; (iv) negation of defense reactions induced by elicitor; and (v) induction of accessibility to fungal invasion.
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