Stomata of most plants close to preserve water when the demand for CO₂ by photosynthesis is reduced. Stomatal responses are slow compared with photosynthesis, and this kinetic difference erodes assimilation and water-use efficiency under fluctuating light. Despite a deep knowledge of guard cells that regulate the stoma, efforts to enhance stomatal kinetics are limited by our understanding of its control by foliar CO₂. Guided by mechanistic modelling that incorporates foliar CO₂ diffusion and mesophyll photosynthesis, here we uncover a central role for endomembrane Ca²⁺ stores in guard cell responsiveness to fluctuating light and CO₂. Modelling predicted and experiments demonstrated a delay in Ca²⁺ cycling that was enhanced by endomembrane Ca²⁺-ATPase mutants, altering stomatal conductance and reducing assimilation and water-use efficiency. Our findings illustrate the power of modelling to bridge the gap from the guard cell to whole-plant photosynthesis, and they demonstrate an unforeseen latency, or ‘carbon memory’, of guard cells that affects stomatal dynamics, photosynthesis and water-use efficiency.

当光合作用对CO ₂的需求减少时，大多数植物的气孔关闭以保存水分。与光合作用相比，气孔反应较慢，并且这种动力学差异会在波动光下侵蚀同化和水分利用效率。尽管对调节气孔的保卫细胞有深入的了解，但增强气孔动力学的努力受到我们对叶面 CO ₂对其控制的理解的限制。在结合叶面 CO ₂扩散和叶肉光合作用的机械模型的指导下，我们在此揭示了内膜 Ca ²⁺储存在保卫细胞对波动光和 CO ₂的反应中的核心作用。建模预测和实验表明 Ca 延迟^{由内膜 Ca 2+ -ATPase 突变体增强的2+}循环，改变气孔导度并降低同化和水分利用效率。我们的研究结果说明了建模能够弥合从保卫细胞到全植物光合作用的差距，并且他们证明了影响气孔动力学、光合作用和水分利用效率的保卫细胞的不可预见的潜伏期或“碳记忆”。