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水分亏缺诱导胁迫乙烯的生物合成。

Biosynthesis of stress ethylene induced by water deficit.

机构信息

Department of Vegetable Crops, University of California, Davis, California 95616.

出版信息

Plant Physiol. 1981 Sep;68(3):594-6. doi: 10.1104/pp.68.3.594.

Abstract

Wheat leaves normally produced very little ethylene, but following a water deficit stress which caused a loss of 9% initial fresh weight, ethylene production increased more than 30-fold within 4 hours and declined rapidly thereafter. The changes in ethylene production were paralleled by an increase and subsequent decrease in 1-aminocyclopropanecarboxylic acid (ACC) content. The level of S-adenosylmethionine was unaffected, suggesting that the conversion of S-adenosylmethionine to ACC is a key reaction in the production of water stress-induced ethylene. This view was further supported by the observation that application of ACC to nonstressed leaf tissue caused a 70-fold increase in ethylene production, while aminoethoxyvinylglycine, a known inhibitor of the conversion of S-adenosylmethionine to ACC, inhibited ACC accumulation as well as the surge in ethylene production if the inhibitor was applied prior to the stress treatment. Cycloheximide, an inhibitor of protein synthesis, effectively blocked both ethylene production and ACC formation, suggesting that water stress induces de novo synthesis of ACC synthase, which is the rate-controlling enzyme in the pathway of ethylene biosynthesis.

摘要

小麦叶片通常产生很少的乙烯,但在水分亏缺胁迫下,初始鲜重损失 9%后,乙烯的产生在 4 小时内增加了 30 多倍,此后迅速下降。乙烯产生的变化与 1-氨基环丙烷羧酸(ACC)含量的增加和随后的减少相平行。S-腺苷甲硫氨酸的水平不受影响,这表明 S-腺苷甲硫氨酸向 ACC 的转化是产生水分胁迫诱导乙烯的关键反应。这一观点得到了进一步的支持,因为向未受胁迫的叶片组织施加 ACC 会导致乙烯产量增加 70 倍,而氨基乙氧基乙烯基甘氨酸是 S-腺苷甲硫氨酸向 ACC 转化的已知抑制剂,如果在胁迫处理前施用抑制剂,它会抑制 ACC 的积累以及乙烯产量的激增。环己亚胺,一种蛋白质合成抑制剂,有效地阻止了乙烯的产生和 ACC 的形成,这表明水分胁迫诱导 ACC 合成酶的从头合成,ACC 合成酶是乙烯生物合成途径中的限速酶。

相似文献

2
Biosynthesis of wound ethylene.创伤乙烯的生物合成
Plant Physiol. 1980 Aug;66(2):281-5. doi: 10.1104/pp.66.2.281.

引用本文的文献

本文引用的文献

1
Biosynthesis of wound ethylene.创伤乙烯的生物合成
Plant Physiol. 1980 Aug;66(2):281-5. doi: 10.1104/pp.66.2.281.

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