Among the modulators of the plant response to pathogens, ethylene (ET) and jasmonic (JA) acid are known to antagonize the effects of salicylic acid (SA). This may be exploited by biotrophic pathogens, including Pseudomonas syringae pv. actinidiae (Psa), responsible for the kiwiplant bacterial canker. In fact, we found a stimulation of ethylene emissions after the infection of micropropagated kiwiplants with Psa. The ethylene emission followed a circadian rithm, being emitted in the dark. The ethylene peaks decreased in intensity during the subsequent days. This pattern appears to be unique to Psa. To prove our hypothesis, and to test possible control methods of Psa in field, plants were treated with Bion® (a structural homologue of SA), ethylene, methyl-jasmonate and successively challenged with Psa inoculation. Bion® significantly reduced the infection, whereas the other treatments gave a neural or negative effect. In conclusion, a model is suggested in which Psa hijack host's defences also by stimulating ethylene emissions to inhibit SA effect. This hypothesis is strengthened by the production by some Psa strains of coronatin, a bacterial toxin acting as a JA homologue. The exogenous stimulation of the SA pathway is effective in limiting the disease severity in field.
Cellini A., Fiorentini L., Vanneste J.L., Cristescu S.M., Harren F.J.M., Costa G., et al. (2012). Induction of ethylene by Pseudomonas syringae pv. actinidiae and its role in the pathogenesis.. AUCKLAND : s.n.
Induction of ethylene by Pseudomonas syringae pv. actinidiae and its role in the pathogenesis.
CELLINI, ANTONIO;FIORENTINI, LUCA;COSTA, GUGLIELMO;SPINELLI, FRANCESCO
2012
Abstract
Among the modulators of the plant response to pathogens, ethylene (ET) and jasmonic (JA) acid are known to antagonize the effects of salicylic acid (SA). This may be exploited by biotrophic pathogens, including Pseudomonas syringae pv. actinidiae (Psa), responsible for the kiwiplant bacterial canker. In fact, we found a stimulation of ethylene emissions after the infection of micropropagated kiwiplants with Psa. The ethylene emission followed a circadian rithm, being emitted in the dark. The ethylene peaks decreased in intensity during the subsequent days. This pattern appears to be unique to Psa. To prove our hypothesis, and to test possible control methods of Psa in field, plants were treated with Bion® (a structural homologue of SA), ethylene, methyl-jasmonate and successively challenged with Psa inoculation. Bion® significantly reduced the infection, whereas the other treatments gave a neural or negative effect. In conclusion, a model is suggested in which Psa hijack host's defences also by stimulating ethylene emissions to inhibit SA effect. This hypothesis is strengthened by the production by some Psa strains of coronatin, a bacterial toxin acting as a JA homologue. The exogenous stimulation of the SA pathway is effective in limiting the disease severity in field.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.