Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259-B-65 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
Plant Mol Biol. 2010 Mar;72(4-5):533-44. doi: 10.1007/s11103-009-9589-4. Epub 2009 Dec 31.
In higher plants, phosphate (Pi) deficiency induces the replacement of phospholipids with the nonphosphorous glycolipids digalactosyldiacylglycerol (DGDG) and sulfoquinovosyldiacylglycerol (SQDG). Genes involved in membrane lipid remodeling are coactivated in response to Pi starvation, but the mechanisms that guide this response are largely unknown. Previously, we reported the importance of auxin transport for DGDG accumulation during Pi starvation. To understand the role of auxin signaling in Arabidopsis membrane lipid remodeling, we analyzed slr-1, a gain-of-function mutant of IAA14 (a repressor of auxin signaling), and arf7arf19, a loss-of-function mutant of auxin response factors ARF7 and ARF19. In slr-1 and arf7arf19, Pi stress-induced accumulation of DGDG and SQDG was suppressed. Reduced upregulation of glycolipid synthase and phospholipase genes in these mutants under Pi-deficient conditions indicates that IAA14 and ARF7/19 affect membrane lipid remodeling at the level of transcription. Pi stress-dependent induction of a non-protein-coding gene, IPS1, was also lower in slr-1 and arf7arf19, whereas expression of At4 (another Pi stress-inducible non-protein-coding gene), anthocyanin accumulation, and phosphodiesterase induction were not reduced in the shoot. High free Pi content was observed in slr-1 and arf7arf19 even under Pi-deficient conditions, suggesting that Pi homeostasis during Pi starvation is altered in these mutants. These results demonstrate a requirement of auxin signaling mediated by IAA14 and ARF7/19 for low-Pi adaptation in Arabidopsis.
在高等植物中,磷酸盐(Pi)缺乏会诱导磷脂被非磷质糖脂二半乳糖基二酰基甘油(DGDG)和磺基奎诺二酰基甘油(SQDG)取代。在响应 Pi 饥饿时,参与膜脂重塑的基因会被协同激活,但指导这种反应的机制在很大程度上是未知的。之前,我们报道了生长素运输对 Pi 饥饿期间 DGDG 积累的重要性。为了了解生长素信号在拟南芥膜脂重塑中的作用,我们分析了 slr-1,这是 IAA14 的功能获得突变体(生长素信号的抑制剂),以及 arf7arf19,生长素响应因子 ARF7 和 ARF19 的功能丧失突变体。在 slr-1 和 arf7arf19 中,Pi 胁迫诱导的 DGDG 和 SQDG 积累受到抑制。在这些突变体中,在 Pi 缺乏条件下糖脂合酶和磷脂酶基因的上调减少表明 IAA14 和 ARF7/19 影响转录水平的膜脂重塑。在 slr-1 和 arf7arf19 中,非蛋白编码基因 IPS1 的 Pi 胁迫依赖性诱导也较低,而 At4(另一种 Pi 胁迫诱导的非蛋白编码基因)的表达、花青素积累和磷酸二酯酶诱导在地上部并未减少。即使在 Pi 缺乏条件下,也观察到 slr-1 和 arf7arf19 中的游离 Pi 含量较高,这表明这些突变体在 Pi 饥饿期间的 Pi 稳态发生改变。这些结果表明生长素信号由 IAA14 和 ARF7/19 介导,是拟南芥适应低 Pi 的必需条件。