State Key Laboratory of Plant Physiology and Biochemistry, College of Life Science, Zhejiang University, Hangzhou, 310058, PR China.
Plant Cell Physiol. 2010 Mar;51(3):380-94. doi: 10.1093/pcp/pcq004. Epub 2010 Jan 12.
In Arabidopsis thaliana, there exist many typical responses to low phosphate (LP) stress, such as inhibition of primary root elongation, proliferation of lateral roots and accumulation of anthocyanin in leaves. The physiological, genetic and molecular mechanisms of these developmental responses remain undefined. We have isolated a phosphorus starvation-insensitive (psi) mutant. The mutant shows impaired inhibition of primary root growth, reduction of root hair growth and reduction of anthocyanin accumulation compared with the wild-type (WT) plants under an LP level. CycB1;1::GUS (cyclin B1;1::beta-glucuronidase) staining suggests that the mutant has a higher ability to maintain cell elongation and cell division than the WT. The genetic analysis and gene cloning indicate that psi is a new allele of lpr1 and that an AC-repeat element in the promoter plays important roles in controlling the expression of LPR1. The psi mutant also shows less sensitivity to auxin treatment compared with the WT and the mutant has an enhanced higher ability to maintain the auxin response in the root tip under LP. However, enhancing the auxin response in the quiescent center cannot mimic the mutant phenotype. These observations suggest that LPR1 is involved in the regulation of the auxin response to Pi starvation and auxin is probably not the only factor affected for maintaining the long-root phenotype under LP stress. Our results also indicate that the function of LPR1 is probably independent of SUMO E3 ligase SIZ1 in response to Pi starvation. The insensitive response of the psi mutant to brefeldin A suggests that LPR1 and PDR2 (Pi Deficiency Response 2) function in opposite ways in regulating the root growth response to Pi starvation in the endoplamic reticulum.
在拟南芥中，存在许多对低磷（LP）胁迫的典型响应，例如抑制主根伸长、侧根增殖和叶片中花色素苷的积累。这些发育响应的生理、遗传和分子机制尚不清楚。我们已经分离到一个对磷饥饿不敏感（psi）的突变体。与野生型（WT）植物相比，该突变体在 LP 水平下表现出抑制主根生长、根毛生长减少和花色素苷积累减少的受损情况。CycB1;1::GUS（细胞周期蛋白 B1;1::β-葡萄糖醛酸酶）染色表明，该突变体比 WT 具有更高的维持细胞伸长和细胞分裂的能力。遗传分析和基因克隆表明，psi 是 lpr1 的一个新等位基因，启动子中的 AC 重复元件在控制 LPR1 的表达中起着重要作用。与 WT 相比，psi 突变体对生长素处理的敏感性也较低，并且在 LP 下，该突变体在根尖维持生长素响应的能力增强。然而，增强静止中心的生长素响应并不能模拟突变体表型。这些观察结果表明，LPR1 参与调节对 Pi 饥饿的生长素响应，生长素可能不是维持 LP 胁迫下长根表型的唯一受影响因素。我们的结果还表明，LPR1 的功能可能独立于 SUMO E3 连接酶 SIZ1 对 Pi 饥饿的响应。psi 突变体对布雷菲德菌素 A 的不敏感反应表明，LPR1 和 PDR2（Pi 缺乏响应 2）在调节对 Pi 饥饿的根生长响应方面以相反的方式发挥作用，内质网。
