SignificanceGuard cells have photosynthetically active chloroplasts in most plant species. However, the significance of their existence in guard cells or their developmental mechanisms is unknown. Here, through a forward-genetic approach, we have identified a key feature and a function of guard cell chloroplasts. We observed that a mutation that impaired chloroplast biogenesis in guard cells also disrupted the regulation of stomatal movements by CO2 and light. We demonstrated that guard cell chloroplasts, compared with those in mesophyll cells, display a unique lipid metabolism, in which the prokaryotic pathway is diminished and the eukaryotic pathway gains control. Our findings highlight the importance of the eukaryotic pathway for developing functional chloroplasts in guard cells.
SUMMARY
An Arabidopsis mutant displaying impaired stomatal responses to CO2, cdi4, was isolated by a leaf thermal imaging screening. The mutated gene PECT1 encodes CTP:phosphorylethanolamine cytidylyltransferase. The cdi4 exhibited a decrease in phosphatidylethanolamine levels and a defect in light‐induced stomatal opening as well as low‐CO2‐induced stomatal opening. We created RNAi lines in which PECT1 was specifically repressed in guard cells. These lines are impaired in their stomatal responses to low‐CO2 concentrations or light. Fungal toxin fusicoccin (FC) promotes stomatal opening by activating plasma membrane H+‐ATPases in guard cells via phosphorylation. Arabidopsis H+‐ATPase1 (AHA1) has been reported to be highly expressed in guard cells, and its activation by FC induces stomatal opening. The cdi4 and PECT1 RNAi lines displayed a reduced stomatal opening response to FC. However, similar to in the wild‐type, cdi4 maintained normal levels of phosphorylation and activation of the stomatal H+‐ATPases after FC treatment. Furthermore, the cdi4 displayed normal localization of GFP‐AHA1 fusion protein and normal levels of AHA1 transcripts. Based on these results, we discuss how PECT1 could regulate CO2‐ and light‐induced stomatal movements in guard cells in a manner that is independent and downstream of the activation of H+‐ATPases. [Correction added on 15 May 2023, after first online publication: The third sentence is revised in this version.]
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