Redox regulation of auxin signaling and plant development in Arabidopsis

Redox regulation of auxin signaling and plant development in Arabidopsis
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DOI:
10.4161/psb.6.1.14203
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发表时间:
2011-01-01
影响因子:
2.9
通讯作者:
Reichheld, Jean-Philippe
Reichheld, Jean-Philippe
中科院分区:
生物学4区
文献类型:
--
作者:
Bashandy, Talaat;Meyer, Yves;Reichheld, Jean-Philippe

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硫氧还蛋白(NTR/TRX)和谷胱甘肽(GSH/GRX)是维持细胞氧化还原稳态的两个主要系统。它们对植物发育、细胞分裂或对环境胁迫的反应至关重要。在最近的一篇文章中,1我们研究了NADP连接的硫氧还蛋白和谷胱甘肽系统之间的相互作用,在生长素信号遗传,通过关联TRX还原酶(ntra ntrb)和谷胱甘肽生物合成(cad 2)突变。我们发现,这两个巯基还原途径干扰发育过程。这是通过调节生长素活性而发生的,如三重ntra ntrb cad 2突变体中功能缺失突变的遗传分析所示。三重突变体在莲座丛阶段几乎正常发育,但未能从花序分生组织产生侧部器官,产生几乎裸露的茎,这让人想起PAT(极性生长素运输)或生物合成中受影响的突变体。三重突变体表现出其他缺陷的过程中,生长素调控,包括顶端优势的损失,脉管系统缺陷和减少次生根生产。此外,它具有较低的生长素(IAA)水平和减少PAT的能力,表明NTR和谷胱甘肽途径通过调节生长素的运输和代谢来影响花序分生组织的发育。
Thioredoxin (NTR/TRX) and glutathione (GSH/GRX) are the two major systems that play a key role in the maintenance of cellular redox homeostasis. They are essential for plant development, cell division or the response to environmental stresses. In a recent article, 1 we studied the interplay between the NADP-linked thioredoxin and glutathione systems in auxin signaling genetically, by associating TRX reductase (ntra ntrb) and glutathione biosynthesis (cad2) mutations. We show that these two thiol reduction pathways interfere with developmental processes. This occurs through modulation of auxin activity as shown by genetic analyses of loss of function mutations in a triple ntra ntrb cad2 mutant. The triple mutant develops almost normally at the rosette stage but fails to generate lateral organs from the inflorescence meristem, producing almost naked stems that are reminiscent of mutants affected in PAT (polar auxin transport) or biosynthesis. The triple mutant exhibits other defects in processes regulated by auxin, including a loss of apical dominance, vasculature defects and reduced secondary root production. Furthermore, it has lower auxin (IAA) levels and decreased capacity for PAT, suggesting that the NTR and glutathione pathways influence inflorescence meristem development through regulation of auxin transport and metabolism.