MOE Key Laboratory of Bioinformatics, Center for Plant Biology, School of Life Sciences, Tsinghua University, Beijing, China.
Plant Signal Behav. 2021 Oct 3;16(10):1946921. doi: 10.1080/15592324.2021.1946921. Epub 2021 Jul 12.
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 encodes an aluminum-activated malate transporter, and its expression is induced by Pi deficiency. In , the expression of is enhanced and the removal of Fe from Pi-deficient medium suppressed the mutant phenotype. In this report, we show that overaccumulates Fe in its root apoplasts, and consequently, produces more hydroxyl radicals, which are detrimental to root growth. Such physiological changes in can be completely suppressed by the mutation of or . 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 expression.
抑制主根 (PR) 生长是拟南芥对磷 (Pi) 缺乏的典型发育反应。已知 SUMO E3 连接酶 SIZ1 的功能失调会增强 Pi 缺乏诱导的 PR 生长抑制。然而,SIZ1 在 Pi 缺乏下如何调节 PR 生长的分子机制尚不清楚。最近有报道称,SIZ1 部分 SUMOylate STOP1,这是一种转录因子,通过调节编码铝激活的苹果酸转运蛋白的表达,在植物对铝毒性的耐受性和对 Pi 缺乏的响应中发挥作用,其表达受 Pi 缺乏诱导。在,的表达增强,并且从缺 Pi 培养基中去除 Fe 抑制了突变体表型。在本报告中,我们表明在其根质外体中积累更多的 Fe,从而产生更多的羟基自由基,这对根生长有害。通过突变或可以完全抑制的这种生理变化。基于以前的研究结果和本研究的结果,我们提出 SIZ1 通过调节 Fe 的积累和通过控制表达来产生羟基自由基来调节 Pi 缺乏介导的 PR 生长。