BHLH32 modulates several biochemical and morphological processes that respond to Pi starvation in Arabidopsis
BHLH32 modulates several biochemical and morphological processes that respond to Pi starvation in Arabidopsis
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DOI：
10.1042/bj20070102
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发表时间：
2007-07-01
影响因子：
4.1
通讯作者：
Nimmo, Hugh G.
中科院分区：
文献类型：
--
作者：
Chen, Zhi-Hui;Nimmo, Gillian A.;Nimmo, Hugh G.
P-i（无机磷酸盐）限制严重损害植物生长并降低作物产量。因此，植物进化出了几种对 P-i 饥饿的生化和形态反应，既增强了吸收，又节省了使用。 P-i 传感和信号转导所涉及的机制尚不完全清楚。在本研究中，我们报道了一种先前未表征的转录因子 BHLH32，在拟南芥中充当一系列 P-i 饥饿诱导过程的负调节因子。在P-i充足条件下的bhlh32突变体植株中，与野生型相比，多个P-i饥饿诱导基因的表达、花青素的形成、总P-i含量和根毛形成均显着增加。 BHLH32 负向调控的基因包括编码 PPCK（磷酸烯醇丙酮酸羧化酶激酶）的基因，该基因参与改变代谢，从而使 P-i 免受影响。本研究表明，P-i 饥饿会快速诱导 PPCK 基因，从而导致磷酸烯醇丙酮酸羧化酶的磷酸化增加。此外，几种调节表皮细胞分化的拟南芥蛋白 [TTG1 (TRANSPARENT TESTA GLABRA1)、GL3 (GLABRA3) 和 EGL3 (ENHANCER OF GL3)] 响应 P-i 饥饿而正向调节 PPCK 基因表达。 BHLH32 可以与 TTG1 和 GL3 发生物理相互作用。我们认为 BHLH32 干扰包含 TTG1 的复合物的功能，从而影响对 P-i 可用性做出反应的几种生化和形态学过程。
P-i (inorganic phosphate) limitation severely impairs plant growth and reduces crop yield. Hence plants have evolved several biochemical and morphological responses to P-i starvation that both enhance uptake and conserve use. The mechanisms involved in P-i sensing and signal transduction are not completely understood. In the present study we report that a previously uncharacterized transcription factor, BHLH32, acts as a negative regulator of a range of P-i starvation-induced processes in Arabidopsis. In bhlh32 mutant plants in P-i-sufficient conditions, expression of several P-i starvation-induced genes, formation of anthocyanins, total P-i content and root hair formation were all significantly increased compared with the wild-type. Among the genes negatively regulated by BHLH32 are those encoding PPCK (phosphoenolpyruvate carboxylase kinase), which is involved in modifying metabolism so that P-i is spared. The present study has shown that PPCK genes are rapidly induced by P-i starvation leading to increased phosphorylation of phosphoenolpyruvate carboxylase. Furthermore, several Arabidopsis proteins that regulate epidermal cell differentiation [TTG1 (TRANSPARENT TESTA GLABRA1), GL3 (GLABRA3) and EGL3 (ENHANCER OF GL3)] positively regulate PPCK gene expression in response to P-i starvation. BHLH32 can physically interact with TTG1 and GL3. We propose that BHLH32 interferes with the function of TTG1-containing complexes and thereby affects several biochemical and morphological processes that respond to P-i availability.