Chen N, Goodwin P H, Hsiang T
Department of Environmental Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
J Exp Bot. 2003 Nov;54(392):2449-56. doi: 10.1093/jxb/erg289.
Two periods of increased ethylene production were observed after inoculation of Nicotiana tabacum by Colletotrichum destructivum. This pathogen exhibits an intracellular hemibiotrophic infection process, with a biotrophic phase followed by a necrotrophic phase. Ethylene production first increased during the biotrophic phase with a peak at 24 h before the necrotrophic phase. A second increase in ethylene occurred late in the necrotrophic phase when the lesions were expanding. Two different 1-aminocyclopropane-1-carboxylic acid synthase genes showed increased expression after the first ethylene peak with a maximum at 24 h before the second ethylene increase. Expression of an 1-aminocyclopropane-1-carboxylic acid oxidase (ACO) gene increased during the first ethylene peak and then declined at the beginning of the second ethylene increase. A second ACO gene showed relatively little change in expression during infection with slightly higher expression at 24 h before the second ethylene increase, and a third ACO gene showed a progressive decline in expression with a major decrease occurring before the second ethylene increase. Inoculation of ethylene-insensitive tobacco with C. destructivum revealed that it was more susceptible than the wild type. The changes in ethylene production and associated gene expression as well as the increased disease susceptibility of ethylene-insensitive tobacco indicate that ethylene plays a role in this interaction, perhaps as a signalling molecule to trigger defense mechanisms.
在用毁灭炭疽菌接种烟草后,观察到两个乙烯产量增加的时期。这种病原菌表现出细胞内半活体营养型感染过程,先有一个活体营养阶段,随后是一个死体营养阶段。乙烯产量在活体营养阶段首先增加,在死体营养阶段前24小时达到峰值。乙烯的第二次增加发生在死体营养阶段后期病斑扩展时。两个不同的1-氨基环丙烷-1-羧酸合酶基因在第一个乙烯峰值后表达增加,在第二次乙烯增加前24小时达到最大值。一个1-氨基环丙烷-1-羧酸氧化酶(ACO)基因的表达在第一个乙烯峰值期间增加,然后在第二次乙烯增加开始时下降。第二个ACO基因在感染期间表达变化相对较小,在第二次乙烯增加前24小时表达略高,第三个ACO基因的表达逐渐下降,在第二次乙烯增加前大幅下降。用毁灭炭疽菌接种乙烯不敏感型烟草发现,它比野生型更易感病。乙烯产量和相关基因表达的变化以及乙烯不敏感型烟草疾病易感性的增加表明,乙烯在这种相互作用中起作用,可能作为一种信号分子触发防御机制。