Biochemical aspects of lipid accumulation in silicon deficient cyclotella cryptica

The experiments described in this report were designed to elucidate the biochemical mechanisms responsible for lipid accumulation in silicon-deficient Cyclotella cryptica T13L cells. Studies using NaH14CO3 as a tracer indicated that the fraction of newly assimilated carbon partitioned into lipids doubled after 4 h of Si deficiency, while the fraction partitioned into chrysolaminarin decreased by 51%. Pulse-chase experiments indicated that a slow redistribution of previously assimilated carbon into lipids also occurred. Several enzymes were assayed in cell-free extracts made from Si-replete and Si-deficient cells. Si deficiency did not affect the specific activity of UDP glucose pyrophosphorylase, the first enzyme of the chrysolaminarin synthesis pathway, but led to a 31% reduction in the activity of chrysolaminarin synthase (UDP glucose: β-1, 3-glucan β-3-glucosyl transferase). The activity of acetyl-CoA carboxylase (the first committed step in lipid biosynthesis) increased by 87% in response to Si deficiency, suggesting either covalent activation or increased levels of this enzyme. The activities of citrate synthase and acetyl-CoA synthetase were not affected by Si deficiency. These results suggest that lipid accumulation in Si deficient cells may be due in part to changes in the activities of chrysolaminarin synthase and acetyl-CoA carboxylase