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从褪绿豌豆切段中快速诱导的伤口乙烯:II. 氧气和温度依赖性。

Rapidly Induced Wound Ethylene from Excised Segments of Etiolated Pisum sativum L., cv. Alaska: II. Oxygen and Temperature Dependency.

机构信息

Department of Horticulture, Michigan State University, East Lansing, Michigan 48824.

出版信息

Plant Physiol. 1978 Apr;61(4):675-9. doi: 10.1104/pp.61.4.675.

Abstract

Wound-induced ethylene synthesis by subapical stem sections of etiolated Pisum sativum L., cv. Alaska seedlings, as described by Saltveit and Dilley (Plant Physiol 1978 61: 447-450), was half-saturated at 3.6% (v/v) O(2) and saturated at about 10% O(2). Corresponding values for CO(2) production during the same period were 1.1% and 10% O(2), respectively. Anaerobiosis stopped all ethylene evolution and delayed the characteristic pattern of wound ethylene synthesis. Exposing tissue to 3.5% CO(2) in air in a flow-through system reduced wound ethylene synthesis by 30%. Enhancing gas diffusivity by reducing the total pressure to 130 mm Hg almost doubled the rate of wound ethylene synthesis and this effect was negated by exposure to 250 mul liter(-1) propylene. Applied ethylene or propylene stopped wound ethylene synthesis during the period of application, but unlike N(2), no lag period was observed upon flushing with air. It is concluded that the characteristic pattern of wound-induced ethylene synthesis resulted from negative feedback control by endogenous ethylene.No wound ethylene was produced for 2 hours after excision at 10 or 38 C. Low temperatures prolonged the lag period, but did not prevent induction of the wound response, since tissue held for 2 hours at 10 C produced wound ethylene immediately when warmed to 30 C. In contrast, temperatures above 36 C prevented induction of wound ethylene synthesis, since tissue cooled to 30 C after 1 hour at 40 C required 2 hours before ethylene production returned to normal levels. The activation energy between 15 and 36 C was 12.1 mole kilocalories degree(-1).

摘要

伤诱导的乙烯合成由子叶下茎切段豌豆(Pisum sativum L. cv. Alaska 幼苗),如 Saltveit 和 Dilley(植物生理学 1978 61:447-450)所述,在 3.6%(v/v)O2 时达到半饱和,在约 10% O2 时达到饱和。在同一时期,CO2 产生的相应值分别为 1.1%和 10% O2。无氧停止了所有乙烯的释放,并延迟了伤诱导的乙烯合成的特征模式。将组织暴露于空气流动系统中的 3.5% CO2 中,可将伤乙烯合成减少 30%。通过将总压力降低到 130 毫米汞柱来增强气体扩散性,几乎使伤乙烯合成速率增加了一倍,而暴露于 250 微升升-1丙烯中则否定了这种效果。施加的乙烯或丙烯在应用期间停止了伤乙烯的合成,但与 N2 不同,在用空气冲洗时没有观察到滞后期。结论是,伤诱导的乙烯合成的特征模式是由内源性乙烯的负反馈控制造成的。在 10 或 38°C 时切除后,2 小时内不会产生伤乙烯。低温延长了滞后期,但并未阻止伤反应的诱导,因为在 10°C 下放置 2 小时的组织在升温至 30°C 时立即产生伤乙烯。相比之下,高于 36°C 的温度会阻止伤乙烯合成的诱导,因为在 40°C 下 1 小时后冷却至 30°C 的组织在乙烯产生恢复正常水平之前需要 2 小时。在 15 至 36°C 之间的激活能为 12.1 毫摩尔千卡度-1。

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