Hormonal regulation of phosphatidylcholine metabolism in Apium graveolens

Abstract

Previous studies using plant growth inhibitors and gibberellic acid led to the hypothesis that two pools of phosphatidylcholine exist within the plant cell; one capable of producing signals involved in cell proliferation and the other capable of releasing signaling molecules which facilitate cell differentiation. It was the aim of this study to extend the current knowledge base through the analysis of phosphatidylcholine metabolism in response to a variety of hormonal signals.
Gibberellin treatment promoted cell elongation, which was accompanied by an increase in the synthesis of cellular phospholipids Metabolic studies involving radiolabelled precursors of phosphatidyicholine, revealed a generalized switching
off of the CDP-choline pathway coupled to a concomitant increase in flux through the phospholipid methyltransferase pathway upon long term exposure to gibberellic acid in conjunction with a decrease in CTP: phosphocholine
cytidylyltransferase activity. Inhibition of phosphatidic acid production in these cultures resulted in a further increase in the flux through the phospholipid methyltransferase pathway.
Jasmonie acid treatment resulted in an increase in cell proliferation coupled with an overall increase in phospholipid and triacyiglycerol synthesis and a decrease in the PC: PE ratio. Short term jasmonic acid treatment, whilst having no effect on
the carbon flux through the phospholipid methyltransferase pathway, led to an increase in carbon flux through the CDP-choline pathway. However, in the long term this effect was diminished, the activity of the CTP: phosphocholine
cytidylyltransferase decreased and an increase in phosphatidyicholine synthesis using methyl moieties occurred. Inhibition of phosphatidic acid by butan-1-ol treatment counteracted the increased labeling of cellular lipids from radiolabelled
methyl donor molecules.
An increase in cell elongation was evoked by abscisic acid treatment. Typically, abscisic acid treated cells contained less phospholipid than their control counterparts. The hormone had little effect on the cellular amounts of triacylglycerols, however an increase in the PC: PE ratio occurred. Short teni abscisic acid treatment resulted in an increase in the incorporation of both radiolabelled choline and methyl groups into cellular lipids. After long term exposure of the cells to abscisic acid, no difference was observed in the overall incorporation of choline and methyl groups into cellular lipids due to a plateau effect being achieved. Treatment with butan-1-ol to reduce phosphatidic acid production had no influence over the functioning of the phospholipid methyltransferase pathway in abscisic acid treated cells.