Abstract

The leaves of monocotyledonous plants create a developmental sequence of cells and plastids from the base to the apical portion. We investigated fatty‐acid and lipid compositions in successive leaf sections of light‐ and dark‐grown wheat (Triticum aestivum L. cv. Chihoku) seedlings. The most notable change in the fatty acid composition was the increase of linolenic acid (18:3) with maturation of leaf cells, which occurred both in light‐ and dark‐grown leaf tissues. In light‐grown leaves, the increase of 18:3 with maturation was mainly attributed to the increase of monogalactosyldiacylglycerol (MGD) and also to the increase of the 18:3 level of MGD. In dark‐grown leaves, the increase of 18:3 in the leaf apex was caused by the increase of the levels of MGD and digalactosyldiacylglycerol (DGD) and also by the increase of the 18:3 levels of within these two lipids. Since MGD and DGD are mainly found in plastid membranes, these findings indicate that both the synthesis of galactolipids and the formation of 18:3 these lipids take place during plastid development. The plastid ω‐3 fatty acid desaturase is responsible for the formation of 18:3 in plastid membrane lipids. To investigate the regulation of desaturation, we isolated a gene for wheat plastid ω‐3 fatty acid desaturase (TaFAD7). The mRNA level of TaFAD7 in light‐grown leaves was much higher than that in dark‐grown leaves. During the greening of etiolated leaves the level of TaFAD7 mRNA increased significantly, accompanied by an increase of the 18:3 level of total fatty acids. On the other hand, the levels of TaFAD7 mRNA were almost the same in all the leaf sections of both light‐ and dark‐grown leaf tissues. These results suggest that the effect of the expression of the TaFAD7 gene on the increase of the 18:3 level is different between the leaf development under continuous light‐ or dark‐conditions and the light‐induced greening process of etiolated leaves. The increase of 18:3 content of MGD (or MGD and DGD) with maturation is apparently regulated not solely by the level of TaFAD7 mRNA.

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