Investigating the mechanisms of sensing and signaling carbon dioxide limitation in the green microalga Chlamydomonas reinhardtii

研究绿色微藻莱茵衣藻感知和发出二氧化碳限制信号的机制

• 批准号: 518659678
• 负责人: Professor Dr. Olaf Kruse
• 金额: --
• 依托单位: Centrum für Biotechnologie (CeBiTec)
• 依托单位国家: 德国
• 项目类别: Research Grants
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/518659678?language=en
• 关键词: Investigating; mechanisms; sensing; signaling; carbon

Adjustment of the light harvesting capacity to light and CO2 supply in phototrophs is a very complex mechanism, operating on distinct time-scales and within different cellular compartments. Prolonged exposure to stress conditions, characterized by an unbalance between light/carbon supply and light capture, triggers long-term acclimation processes, which are accompanied by a modulated gene expression and hence stoichiometric adjustments of the photosynthetic machinery, ensuring unperturbed continuation of carbon fixation. In phototrophic eukaryotes, a prime target of these adjustments are nucleus-encoded light-harvesting proteins associated with photosystem II (LHCBM). A sudden drop in CO2 availability increases excitation pressure at photosystem II and immediately activates non-photochemical quenching (NPQ) mechanisms like state transitions to relieve it quickly. Prolonged limitation, however, leads to a relaxation of NPQ and a replacement of these short-term acclimation mechanisms by long-term responses, like functional antenna size truncation. In a previous DFG project, it was demonstrated that antenna size truncation mechanistically relies on LHCBM translation repression, which efficiently relieves excitation pressure. The whole process relied on an accumulation of the translation repressor NAB1 via activation of its nuclear promoter, which was dependent on a plastid retrograde signal implicating photosynthetic electron transfer. At the centre of this novel regulatory circuit is the newly identified transcription factor LCRF (low carbon dioxide response factor), which is induced by low carbon dioxide supply and crucial for NAB1 promoter activation. Exploiting the identified model pathway, we will investigate how a microalga senses CO2 limitation and how this is signaled to the nucleus by identifying novel components involved in the process of modulating photosynthetic gene expression.

在光养生物中，光捕获能力对光和二氧化碳供应的调节是一个非常复杂的机制，在不同的时间尺度上和在不同的细胞隔间内运行。长期暴露在胁迫条件下，以光/碳供应和光捕获之间的失衡为特征，会触发长期的适应过程，伴随着基因表达的调节，从而对光合作用机制进行化学计量调整，确保不受干扰地继续固碳。在光养真核生物中，这些调节的主要靶点是与光系统II(LHCBM)相关的核编码的捕光蛋白。二氧化碳可获得性的突然下降增加了光系统II的激发压力，并立即激活非光化学猝灭(NPQ)机制，如状态转换，以迅速缓解它。然而，长时间的限制会导致NPQ的放松，并用长期反应取代这些短期适应机制，如功能天线尺寸截断。在以前的DFG项目中，已经证明了天线尺寸截断机械地依赖于LHCBM平移抑制，从而有效地缓解了激励压力。整个过程依赖于翻译抑制物NAB1通过其核启动子的激活而积累，这依赖于涉及光合作用电子传递的叶绿体逆行信号。在这个新的调控电路的中心是新发现的转录因子LCRF(低二氧化碳反应因子)，它是由低二氧化碳供应诱导的，对NAB1启动子的激活至关重要。利用已识别的模型途径，我们将通过识别参与调节光合作用基因表达过程的新成分，来研究微藻如何感知二氧化碳限制以及这是如何向细胞核发送信号的。