ABSTRACT

Inhibition of primary root (PR) growth is a typical developmental response of Arabidopsis to phosphate (Pi) deficiency. Functional disruption of SIZ1, a SUMO E3 ligase, is known to enhance the Pi deficiency-induced inhibition of PR growth. The molecular mechanism of how SIZ1 regulates PR growth under Pi deficiency, however, remains unknown. SIZ1 was recently reported to partially SUMOylate STOP1, a transcription factor that functions in plant tolerance to aluminum toxicity and in plant responses to Pi deficiency by regulating the expression of ALMT1. ALMT1 encodes an aluminum-activated malate transporter, and its expression is induced by Pi deficiency. In siz1, the expression of ALMT1 is enhanced and the removal of Fe from Pi-deficient medium suppressed the siz1 mutant phenotype. In this report, we show that siz1 overaccumulates Fe in its root apoplasts, and consequently, produces more hydroxyl radicals, which are detrimental to root growth. Such physiological changes in siz1 can be completely suppressed by the mutation of STOP1 or ALMT1. Based on previously published work and the results of the current study, we propose that SIZ1 regulates Pi deficiency-mediated PR growth through modulating the accumulation of Fe and the production of hydroxyl radicals by controlling ALMT1 expression.

摘要

抑制初生根 (PR) 生长是拟南芥对磷酸盐 (Pi) 缺乏的典型发育反应。已知 SIZ1（一种 SUMO E3 连接酶）的功能破坏会增强 Pi 缺乏诱导的 PR 生长抑制。然而，SIZ1 如何在 Pi 缺乏的情况下调节 PR 生长的分子机制仍然未知。最近报道 SIZ1 部分 SUMOylate STOP1，一种转录因子，通过调节 ALMT1 的表达在植物对铝毒性的耐受性和植物对磷缺乏的反应中发挥作用。ALMT1编码一种铝激活的苹果酸转运蛋白，其表达是由 Pi 缺乏诱导的。在siz1中， ALMT1的表达增强，并且从 Pi 缺乏的培养基中去除 Fe 抑制了siz1突变体表型。在本报告中，我们表明siz1在其根质外体中过度积累铁，因此产生更多的羟基自由基，这对根系生长有害。STOP1或ALMT1的突变可以完全抑制siz1的这种生理变化。基于先前发表的工作和当前研究的结果，我们提出 SIZ1 通过调节 Fe 的积累和通过控制ALMT1表达来调节羟基自由基的产生来调节 Pi 缺乏介导的 PR 生长。