Kobayashi Koichi, Masuda Tatsuru, Takamiya Ken-Ichiro, Ohta Hiroyuki
Department of Bioscience, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259-B-14 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
Plant J. 2006 Jul;47(2):238-48. doi: 10.1111/j.1365-313X.2006.02778.x. Epub 2006 Jun 7.
During phosphate (Pi) starvation in plants, membrane phospholipid content decreases concomitantly with an increase in non-phosphorus glycolipids. Although several studies have indicated the involvement of phytohormones in various physiological changes upon Pi starvation, the regulation of Pi-starvation induced membrane lipid alteration remains unknown. Previously, we reported the response of type B monogalactosyl diacylglycerol synthase genes (atMGD2 and atMGD3) to Pi starvation, and suggested a role for these genes in galactolipid accumulation during Pi starvation. We now report our investigation of the regulatory mechanism for the response of atMGD2/3 and changes in membrane lipid composition to Pi starvation. Exogenous auxin activated atMGD2/3 expression during Pi starvation, whereas their expression was repressed by cytokinin treatment in the root. Moreover, auxin inhibitors and the axr4 aux1 double mutation in auxin signaling impaired the increase of atMGD2/3 expression during Pi starvation, showing that auxin is required for atMGD2/3 activation. The fact that hormonal effects during Pi starvation were also observed with regard to changes in membrane lipid composition demonstrates that both auxin and cytokinin are indeed involved in the dynamic changes in membrane lipids during Pi starvation. Phosphite is not metabolically available in plants; however, when we supplied phosphite to Pi-starved plants, the Pi-starvation response disappeared with respect to both atMGD2/3 expression and changes in membrane lipids. These results indicate that the observed global change in plant membranes during Pi starvation is not caused by Pi-starvation induced damage in plant cells but rather is strictly regulated by Pi signaling and auxin/cytokinin cross-talk.
在植物磷饥饿期间，膜磷脂含量会随着非磷糖脂的增加而相应减少。尽管多项研究表明植物激素参与了磷饥饿时的各种生理变化，但磷饥饿诱导的膜脂改变的调控机制仍不清楚。此前，我们报道了B型单半乳糖基二酰甘油合酶基因（atMGD2和atMGD3）对磷饥饿的响应，并提出这些基因在磷饥饿期间半乳糖脂积累中发挥作用。我们现在报告对atMGD2/3响应以及膜脂组成变化对磷饥饿的调控机制的研究。外源生长素在磷饥饿期间激活了atMGD2/3的表达，而在根中细胞分裂素处理则抑制了它们的表达。此外，生长素抑制剂以及生长素信号传导中的axr4 aux1双突变削弱了磷饥饿期间atMGD2/3表达的增加，表明生长素是激活atMGD2/3所必需的。在膜脂组成变化方面也观察到磷饥饿期间的激素效应，这表明生长素和细胞分裂素确实都参与了磷饥饿期间膜脂的动态变化。亚磷酸盐在植物中无法进行代谢利用；然而，当我们向缺磷植物供应亚磷酸盐时，缺磷响应在atMGD2/3表达和膜脂变化方面均消失。这些结果表明，在磷饥饿期间观察到的植物膜的整体变化不是由磷饥饿诱导的植物细胞损伤引起的，而是由磷信号传导以及生长素/细胞分裂素相互作用严格调控的。
