光系统II组装因子RBD1和HCF136的对立作用是植物质体中光调节的psbA转化背后的原因
Margarita Rojas1, Rosalind Williams-Carrier1, Prakitchai Chotewutmontri1
1Institute of Molecular Biology, University of Oregon, Eugene, OR 97403.
概括
光系统II (PSII) 受到的光损伤触发了叶绿体psbAmRNA的翻译,用于D1蛋白修复. RBD1通过抑制HCF136来激活这个过程,而HCF244则独立地招募核糖体.
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.
- 叶绿体基因表达调节调节基因表达调节
背景情况:
- 光系统II (PSII) 中的D1蛋白容易受到光损伤.
- 叶绿体psbAmRNA翻译为PSII修复提供了新的D1.
- 组装因子HCF244,RBD1和HCF136都与psbA的翻译调节有关.
研究的目的:
- 为了阐明 psbA mRNA 翻译响应D1光损伤的调节电路.
- 为了澄清HCF244,RBD1和HCF136在psbA翻译控制中的不同作用.
- 为了确定将D1光损伤与D1合成调节联系在一起的信号机制.
主要方法:
- 在Arabidopsis和玉米突变体中分析psbA核糖体占用率.
- 研究的rbd1,rbd1;hcf136,Zm-hcf244和Zm-hcf244;Zm-hcf136双重突变物.这些突变物中,有两种突变物.
- 评估了HCF244在HCF173与psbA 5'UTR结合中的作用.
主要成果:
- RBD1对于光诱导的psbA转化至关重要,通过抑制HCF136抑制而起作用.
- 在任何条件下,HCF244是需要用于核糖体招募到psbAmRNA的.
- HCF244的功能是在HCF173结合的下游,不需要HCF173.
结论:
- RBD1感知到D1的光损伤,并通过缓解HCF136介导的抑制来激活psbA翻译.
- HCF244的作用是下游的,促进了独立于HCF173.3的核糖体招募.
- 一个由HCF136和RBD1调节的新兴D1特征,信号D1光损伤,以调节PSII修复的psbA翻译.
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