PECT1, a rate-limiting enzyme in phosphatidylethanolamine biosynthesis, is involved in the regulation of stomatal movement in Arabidopsis

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 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.

Automated summary

A mutant of Arabidopsis, cdi4, was found to have impaired stomatal responses to CO2 and light. This mutation is associated with a gene called PECT1, which encodes CTP:phosphorylethanolamine cytidylyltransferase. By suppressing the expression of PECT1 in guard cells, it was discovered that these mutant lines also exhibited impaired stomatal responses to low-CO2 concentrations or light.