The role of ethylene during the infection of Nicotiana tabacum by Colletotrichum destructivum
The role of ethylene during the infection of Nicotiana tabacum by Colletotrichum destructivum
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DOI：
10.1093/jxb/erg289
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发表时间：
2003-11-01
影响因子：
6.9
通讯作者：
Hsiang, T
中科院分区：
文献类型：
--
作者：
Chen, N;Goodwin, PH;Hsiang, T
烟草接种炭疽菌后，乙烯产生量有两个增加时期。该病原体表现出细胞内半活体营养型感染过程，活体营养期之后是坏死营养期。乙烯的产生首先增加，在活体营养阶段的峰值在24小时前的坏死营养阶段。乙烯的第二次增加发生在坏死营养期后期，此时病变正在扩大。两个不同的1-氨基环丙烷-1-羧酸合酶基因表现出增加的表达后，第一个乙烯峰值，在24小时前的第二个乙烯增加的最大值。1-氨基环丙烷-1-羧酸氧化酶（ACO）基因的表达在第一次乙烯高峰期间增加，然后在第二次乙烯增加开始时下降。第二个ACO基因表现出相对较小的变化，在感染过程中的表达略高，在第二次乙烯增加前24小时的表达，和第三ACO基因表现出一个渐进的下降，在第二次乙烯增加前发生的主要减少表达。用C. destructivum表明它比野生型更敏感。乙烯产生和相关基因表达的变化以及乙烯不敏感烟草对疾病易感性的增加表明乙烯在这种相互作用中起作用，可能作为触发防御机制的信号分子。
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.