Regulation of phosphate homeostasis by microRNA in Arabidopsis
Regulation of phosphate homeostasis by microRNA in Arabidopsis
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DOI：
10.1105/tpc.105.038943
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发表时间：
2006-02-01
期刊：
影响因子：
11.6
通讯作者：
Su, CL
中科院分区：
文献类型：
--
作者：
Chiou, TJ;Aung, K;Su, CL
在这项研究中，我们揭示了一种机制，植物调节无机磷（Pi）的稳态，以适应环境变化的Pi可用性。这种机制涉及通过特定的microRNA miR399抑制泛素缀合的E2酶。在Pi饥饿时，miR399在拟南芥中上调，而其靶基因泛素缀合E2酶在拟南芥中下调。在过表达miR399的转基因拟南芥中，E2转录物的积累受到抑制。转基因植物在芽中积累的Pi水平是正常Pi水平的五到六倍，并表现出Pi毒性症状，这些症状被功能丧失的E2突变体表型模仿。磷毒是由于磷的吸收增加，磷从根转移到地上部，并滞留在地上部。此外，与野生型植物不同，其中老叶中的Pi容易重新定位到其他发育中的年轻组织，miR 399过表达植物中Pi的再动员受损。这些结果提供了证据表明，miRNA控制Pi的稳态通过调节植物中的蛋白水解机制的一个组件的表达。
In this study, we reveal a mechanism by which plants regulate inorganic phosphate ( Pi) homeostasis to adapt to environmental changes in Pi availability. This mechanism involves the suppression of a ubiquitin-conjugating E2 enzyme by a specific microRNA, miR399. Upon Pi starvation, the miR399 is upregulated and its target gene, a ubiquitin-conjugating E2 enzyme, is downregulated in Arabidopsis thaliana. Accumulation of the E2 transcript is suppressed in transgenic Arabidopsis overexpressing miR399. Transgenic plants accumulated five to six times the normal Pi level in shoots and displayed Pi toxicity symptoms that were phenocopied by a loss-of-function E2 mutant. Pi toxicity was caused by increased Pi uptake and by translocation of Pi from roots to shoots and retention of Pi in the shoots. Moreover, unlike wild-type plants, in which Pi in old leaves was readily retranslocated to other developing young tissues, remobilization of Pi in miR399-overexpressing plants was impaired. These results provide evidence that miRNA controls Pi homeostasis by regulating the expression of a component of the proteolysis machinery in plants.