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矮牵牛花朵早期雌蕊乙烯对加速萎蔫缺乏调控作用。

Lack of Control by Early Pistillate Ethylene of the Accelerated Wilting of Petunia hybrida Flowers.

作者信息

Hoekstra F A, Weges R

机构信息

Department of Plant Physiology, Agricultural University, Arboretumlaan 4, 6703 BD Wageningen, The Netherlands.

出版信息

Plant Physiol. 1986 Feb;80(2):403-8. doi: 10.1104/pp.80.2.403.

Abstract

Well before pollen tube penetration, ethylene has begun to disseminate from pollinated styles of Petunia hybrida flowers. Previous stigmatic application of aminoethoxyvinylglycine (AVG) completely prevented this ethylene synthesis, indicating that the endogenous 1-aminocyclopropane-1-carboxylic acid (ACC) in pollen is not readily converted on the stigma. Compared to other flower parts, the capacity of the ethylene forming enzyme was largest in the stigma. When applied to the stigma, ACC caused ethylene synthesis, but did not accelerate wilting, unless high concentrations (20 nanomols) were used. Upon pollination or stigma wounding, the early ethylene evolved exclusively from the gynoecium, much later followed by the synthesis of corolla ethylene. Employing wideneck Erlenmeyer flasks, the competitive inhibitor of ethylene action, norbornadiene, was applied to entire flowers in situ, with delaying effects on wound-induced wilting. In contrast, norbornadiene treatment of styles alone, using capillaries, could not postpone wilting. Pollination with foreign pollen species did not lead to accelerated corolla wilting, notwithstanding considerable synthesis of ethylene during the first 5 hours. In situ treatment of the stigma with AVG considerably delayed wound- and pollination-induced wilting. Removal of the entire AVG-treated style 6 hours after stigma wounding still allowed for the postponement of the accelerated wilting, even at very low concentrations of AVG. It is concluded that early stylar ethylene does not play a role in the acceleration of wilting but that, much later, corolla ethylene does, induced by a mobile wilting factor from the stigma, which is ACC.

摘要

早在花粉管穿透之前,乙烯就已开始从矮牵牛花朵授粉后的花柱中扩散出来。先前在柱头上施用氨基乙氧基乙烯基甘氨酸(AVG)完全阻止了这种乙烯的合成,这表明花粉中的内源性1-氨基环丙烷-1-羧酸(ACC)在柱头上不易转化。与其他花部相比,乙烯形成酶在柱头中的活性最大。当将ACC施用于柱头时,会引起乙烯合成,但不会加速枯萎,除非使用高浓度(20纳摩尔)。授粉或柱头受伤后,早期乙烯仅从雌蕊中释放出来,很久之后花冠乙烯才开始合成。使用广口锥形瓶,将乙烯作用的竞争性抑制剂降冰片二烯原位施用于整朵花,对伤口诱导的枯萎有延迟作用。相比之下,单独使用毛细管对花柱进行降冰片二烯处理并不能推迟枯萎。用外来花粉品种授粉不会导致花冠加速枯萎,尽管在最初的5小时内乙烯大量合成。用AVG对柱头进行原位处理可大大延迟伤口和授粉诱导的枯萎。柱头受伤6小时后去除整个用AVG处理过的花柱,即使在非常低的AVG浓度下,仍可推迟加速枯萎。得出的结论是,早期花柱乙烯在加速枯萎过程中不起作用,但很久之后,花冠乙烯起作用,它是由来自柱头的一种可移动的枯萎因子ACC诱导产生的。

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