Figure 7.

A proposed model of the timing of biochemical changes in LT-induced phenotypes of tocopherol-deficient mutants. Tocopherol deficiency, e.g., by the vte2 mutation, leads to constitutive alterations in the fatty acid composition of endoplasmic reticulum (ER) membrane lipids [i.e., reduced linolenic acid (18:3) and increased linoleic acid (18:2)]. These alterations are suppressed by the mutation of the ER FATTY ACID DESATURASE 2 gene (fad2), which also suppresses all of the LT-induced vte2 phenotypes (Maeda et al., 2008; Song et al., 2010). Subsequent vasculature-specific callose deposition is primarily mediated by the GSL5 enzyme and tocopherol-deficiency affects its activity post-transcriptionally. Although low levels of GSL5-independent callose deposition still occurs, loss of the massive GSL5-dependent callose deposition in transfer cells does not affected the subsequent defect in photoassimilate export in LT-treated vte2.