改变的脂酸乙烯链长度控制了光采集复杂II蛋白质体的能量消耗,通过疏水不匹配
Dan-Hong Li1, Sam Wilson1, Giulia Mastroianni1
1Department of Biochemistry, School of Biological and Behavioural Sciences, Queen Mary University of London, London E1 4NS, United Kingdom.
Journal of photochemistry and photobiology. B, Biology
|August 2, 2023
概括
植物光采集复合体 (LHCII) 使用疏水不匹配转换到光保护状态. 在蛋白质体中改变脂酸链长度证实了这一机制,影响了LHCII光.
科学领域:
- 植物分子生物学 植物分子生物学
- 光合作用研究研究光合作用.
- 膜生物物理学 膜生物物理学
背景情况:
- 主光采集天线综合体 (LHCII) 对于光系统II中的光采集和光保护至关重要.
- 对于LHCII光保护 (qE) 的一种拟议机制涉及甲状腺膜内的疏水不匹配.
- 之前已经观察到由ΔpH诱导的膜稀释,这表明膜性质的作用.
研究的目的:
- 实验验证水不匹配在调节LHCII光保护中的作用.
- 研究脂酸链长度 (ACL) 的变化如何影响LHCII功能和形状.
- 为了确定膜厚度的变化是否可以诱导LHCII火.
主要方法:
- 使用具有不同乙烯链长度 (ACL) 的脂质构建蛋白质体.
- 测量了LHCII在这些蛋白质体内的平均叶绿素光寿命.
- 对77K光光谱进行分析,以描述LHCII形状.
主要成果:
- 脂质ACL显著影响LHCII的平均色素光寿命.
- 一个18个碳的ACL产生了光寿命 (∼2 ns),与本地甲状腺膜相比.
- 在LHCII表现出灭的光在proteoliposomes与ACL短或长于18碳,表明改变的构造.
结论:
- 这项研究支持了由膜厚度 (ACL) 变化驱动的疏水不匹配触发LHCII光保护 (qE) 的假设.
- 减少ACL导致LHCII的明显灭形状,类似于聚合或固定状态.
- 这些发现为膜脂质特性在调节光合作用光管理中的作用提供了直接证据.
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