The aim of this work was to discover why pea (Pisum sativum L.) embryos recessive at the r locus (rr) have a higher lipid content than embryos dominant at this locus (RR). The r locus is a gene encoding starchbranching enzyme, rr embryos have a much lower activity of this enzyme than RR embryos, and hence a reduced rate of starch synthesis. The higher lipid content of rr embryos must be a consequence of this. We suggest that neither differences in the availability of substrate for lipid synthesis as a consequence of different rates of starch synthesis, nor differences in the capacity of the pathway for malonyl-CoA synthesis, account for the different lipid contents of RR and rr embryos. Lipid contents of the two sorts of embryo first diverge at a much later stage in development than divergence in starch content. Amounts of pyruvate and acetate, and activities of enzymes that convert triose phosphate to malonyl CoA are the same in the two sorts of embryo. Most of the lipid in developing embryos is polar, structural lipid, and polar lipid accounts for a large proportion of the difference in lipid content between the two sorts of embryo. This difference in structural-lipid content reflects considerable structural differences between the two sorts of embryo and is presumably the consequence of differences in rates of lipid turnover.