Tao Sibo, Zhang Ye, Wang Xiaoyue, Xu Le, Fang Xiaofeng, Lu Zhi John, Liu Dong
MOE Key Laboratory of Bioinformatics, Center for Plant Biology, School of Life Sciences, Tsinghua University, Beijing 100084, China.
MOE Key Laboratory of Bioinformatics, Center for Plant Biology, School of Life Sciences, Tsinghua University, Beijing 100084, China
Plant Physiol. 2016 Aug;171(4):2841-53. doi: 10.1104/pp.16.00680. Epub 2016 Jun 21.
Induction and secretion of acid phosphatases (APases) is an adaptive response that plants use to cope with P (Pi) deficiency in their environment. The molecular mechanism that regulates this response, however, is poorly understood. In this work, we identified an Arabidopsis (Arabidopsis thaliana) mutant, hps8, which exhibits enhanced APase activity on its root surface (also called root-associated APase activity). Our molecular and genetic analyses indicate that this altered Pi response results from a mutation in the AtTHO1 gene that encodes a subunit of the THO/TREX protein complex. The mutation in another subunit of this complex, AtTHO3, also enhances root-associated APase activity under Pi starvation. In Arabidopsis, the THO/TREX complex functions in mRNA export and miRNA biogenesis. When treated with Ag(+), an inhibitor of ethylene perception, the enhanced root-associated APase activity in hps8 is largely reversed. hpr1-5 is another mutant allele of AtTHO1 and shows similar phenotypes as hps8 ein2 is completely insensitive to ethylene. In the hpr1-5ein2 double mutant, the enhanced root-associated APase activity is also greatly suppressed. These results indicate that the THO/TREX complex in Arabidopsis negatively regulates root-associated APase activity induced by Pi starvation by inhibiting ethylene signaling. In addition, we found that the miRNA399-PHO2 pathway is also involved in the regulation of root-associated APase activity induced by Pi starvation. These results provide insight into the molecular mechanism underlying the adaptive response of plants to Pi starvation.
酸性磷酸酶（APases）的诱导和分泌是植物应对环境中磷（Pi）缺乏的一种适应性反应。然而，调节这种反应的分子机制却知之甚少。在这项研究中，我们鉴定出一个拟南芥（Arabidopsis thaliana）突变体hps8，其根表面的APase活性增强（也称为根相关APase活性）。我们的分子和遗传分析表明，这种改变的Pi反应是由编码THO/TREX蛋白复合体一个亚基的AtTHO1基因突变引起的。该复合体另一个亚基AtTHO3的突变，在Pi饥饿条件下也会增强根相关APase活性。在拟南芥中，THO/TREX复合体在mRNA输出和miRNA生物合成中发挥作用。用乙烯感知抑制剂Ag(+)处理后，hps8中增强的根相关APase活性在很大程度上得以逆转。hpr1-5是AtTHO1的另一个突变等位基因，表现出与hps8相似的表型，ein2对乙烯完全不敏感。在hpr1-5ein2双突变体中，增强的根相关APase活性也受到极大抑制。这些结果表明，拟南芥中的THO/TREX复合体通过抑制乙烯信号传导，负向调节Pi饥饿诱导的根相关APase活性。此外，我们发现miRNA399-PHO2途径也参与了Pi饥饿诱导的根相关APase活性的调节。这些结果为植物对Pi饥饿适应性反应的分子机制提供了深入了解。
