Mechanisms of Light Regulated Translation in Chloroplasts

该项目解决了生物学中的一个基本问题：生物体如何调节基因表达以适应环境波动？它的重点是光对光合作用所需蛋白质合成的影响，光合作用是一种消耗大气中的二氧化碳并产生为生命提供燃料的碳水化合物的过程。光驱动光合作用，但也会破坏光合作用装置。损伤的修复需要用新合成的蛋白质替换受损的部分。该项目研究了破坏光合装置的同一光线如何激活修复所需的新蛋白质的合成。对这种修复机制的理解对作物在面对不断变化的环境条件时的生产力和恢复力具有重要意义。高中生、高中教师和本科生将通过参与本项目获得研究实践经验。光损伤的主要目标是一种名为D1的蛋白质，它位于光系统II （PSII）中，由psbA基因编码。D1的合成速率随着光强的增加而增加，为PSII修复提供D1。在叶绿体中，这种调节发生在翻译水平上。先前的研究揭示了光诱导的D1损伤、psbA mRNA特异性核糖体的募集以及类囊体膜中介导PSII组装和修复的保守蛋白复合物之间的密切联系。这项工作最终建立了一个模型，该模型调用组装/修复复合体作为翻译自动调节机制的中心，该机制将psbA的翻译与D1在光诱导损伤后的需求结合起来。实验将测试和阐述这一机制，重点关注膜结合组装复合物和基质中结合psbA mRNA的翻译激活剂之间的通信。实验将采用多方面的遗传，分子，基因组和生化方法在玉米和拟南芥。该奖项反映了美国国家科学基金会的法定使命，并通过使用基金会的知识价值和更广泛的影响审查标准进行评估，被认为值得支持。

This project addresses a fundamental question in biology: How do organisms regulate gene expression to adapt to environmental fluctuations? It focuses on effects of light on the synthesis of proteins required for photosynthesis, a process that consumes atmospheric CO2 and produces the carbohydrates that fuel life. Light drives photosynthesis, but it also damages the photosynthetic apparatus. Repair of the damage requires the replacement of damaged parts with newly synthesized proteins. This project examines how the same light that damages the photosynthetic apparatus also activates the synthesis of new proteins required for repair. An understanding of this repair mechanism has implications for crop productivity and resilience in the face of changing environmental conditions. High school students, high school teachers, and undergraduate students will gain hands-on experience with research through involvement in this project. The primary target of photodamage is a protein called D1, which resides in Photosystem II (PSII) and is encoded by the psbA gene. The rate of D1 synthesis increases with light intensity to provide D1 for PSII repair. In chloroplasts, this regulation occurs at the level of translation. Prior work revealed an intimate connection between light-induced D1 damage, the recruitment of ribosomes specifically to psbA mRNA, and a conserved protein complex in the thylakoid membrane that mediates PSII assembly and repair. This work culminated in a model that invokes the assembly/repair complex as the hub of a translational autoregulatory mechanism that couples psbA translation to the need for D1 following its light-induced damage. Experiments will test and elaborate on this proposed mechanism, with a focus on communication between the membrane-bound assembly complex and a translational activator in the stroma that binds psbA mRNA. Experiments will employ multifaceted genetic, molecular, genomic, and biochemical approaches in maize and Arabidopsis.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.