SummaryPost-germinative growth of oilseeds is dependent on the breakdown of the stored lipid reserves. Long-chain acyl-CoA synthetase activities (LACS) are critically involved in this process by activating the released free fatty acids and thus feeding the b-oxidation cycle in glyoxysomes. Here we report on the identification of two LACS genes, AtLACS6 and AtLACS7 from Arabidopsis thaliana coding for peroxisomal LACS proteins. The subcellular localization was verified by co-expression studies of spectral variants of the green fluorescent protein (GFP). While AtLACS6 is targeted by a type 2 (PTS2) peroxisomal targeting sequence, for AtLACS7 a functional PTS1 as well as a PTS2 could be demonstrated. Possible explanations for this potentially redundant targeting information will be discussed. Expression studies of both genes revealed a strong induction 1 day after germination resembling the expression pattern of other genes involved in b-oxidation. Analysis of the substrate specificities of the two LACS proteins demonstrated enzymatic activity for both enzymes with the whole spectrum of fatty acids found in stored lipid reserves. These results suggest that both LACS proteins might have overlapping functions and are able to initiate b-oxidation in plant peroxisomes.

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Upon transfer of a genetically engineered Escherichia coli gene for glycerol‐3‐phosphate acyltransferase (plsB) to Arabidopsis thaliana (L.) Heynh., the gene is transcribed and translated into an enzymatically active polypeptide. This leads to an alteration in fatty acid composition of membrane lipids. From these alterations it is evident that the enzyme is located mainly inside the plastids. The amount of saturated fatty acids in plastidial membrane lipids increased. In particular, the fraction of high‐temperature melting species of phosphatidylglycerol is elevated. These molecules are thought to play a crucial role in determining chilling sensitivity of plants. An increase in sensitivity could be observed in the transgenic plants during recultivation after chilling treatment. Implications for the hypothesis of phosphatidylglycerol‐determined chilling sensitivity are discussed.