Mutations of the ER to plastid lipid transporters TGD1, 2, 3 and 4 and the ER oleate desaturase FAD2 suppress the low temperature-induced phenotype of Arabidopsis tocopherol-deficient mutant vte2.

Previous studies with the tocopherol-deficient Arabidopsis thaliana vte2 mutant demonstrated an important role for tocopherols in the development of transfer cell walls and maintenance of photoassimilate export capacity during low-temperature (LT) adaptation. To further understand the processes linking tocopherol deficiency and the vte2 LT phenotypes, a genetic screen was performed for sve mutations (suppressor of the vte2 low temperature-induced phenotype). The three strongest sve loci had differing impacts on LT-induced sugar accumulation, photoassimilate export reduction and vascular-specific callose deposition in vte2. sve1 completely suppressed all vte2 LT phenotypes and is a new allele of fad2, the endoplasmic reticulum-localized oleate desaturase. sve2 showed partial suppression, and is a new allele of trigalactosyldiacylglycerol1 (tgd1), a component of the ER-to-plastid lipid ATP-binding cassette (ABC) transporter. Introduction of tgd2, tgd3 and tgd4 mutations into the vte2 background similarly suppressed the vte2 LT phenotypes, indicating a key role for ER-to-plastid lipid transport in the vte2 LT phenotype. sve7 partially suppressed all vte2 LT phenotypes by affecting fatty acid and lipid metabolism at low temperatures only. Detailed analyses of acyl lipid composition indicated that all suppressors alleviated the increase in the level of linoleic acid esterified to phosphatidylcholine (PC-18:2) in LT-treated vte2, and this alleviation significantly correlated with their extent of suppression of photoassimilate export. Identification and characterization of the sve loci showed that the PC-18:2 change is an early and key component in vte2 LT-induced responses, and highlighted the interaction of tocopherols with non-plastid lipid metabolism.