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

光养生物对光和CO2供应的捕光能力的调节是一个非常复杂的机制，在不同的时间尺度上和不同的细胞隔室中操作。长时间暴露于应激条件下，其特征在于光/碳供应和光捕获之间的不平衡，触发长期的适应过程，这伴随着调制的基因表达，因此光合机制的化学计量调整，确保碳固定的不受干扰的持续。 在光养真核生物中，这些调节的主要目标是与光系统II（LHCBM）相关的核编码捕光蛋白。CO2可用性的突然下降会增加光系统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，以快速缓解。然而，长期的限制，导致放松NPQ和长期的反应，如功能天线大小截断这些短期的适应机制的替代。在之前的DFG项目中，已经证明了天线尺寸截断机制依赖于LHCBM翻译抑制，这有效地缓解了激发压力。整个过程依赖于翻译抑制因子NAB 1通过其核启动子的激活而积累，这依赖于涉及光合电子传递的质体逆行信号。在这个新的调节回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NAB 1启动子激活至关重要。利用所确定的模型途径，我们将研究一个microplastics传感器如何CO2限制，以及如何通过识别参与调节光合基因表达过程的新组件向细胞核发出信号。

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.