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Article Abstract

An Arabidopsis mutant displaying impaired stomatal responses to CO , 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-CO -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-CO 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 CO - 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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http://dx.doi.org/10.1111/tpj.16245DOI Listing

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