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首页> 外文期刊>Journal of Experimental Botany >Aluminium-induced inhibition of root elongation in Arabidopsis is mediated by ethylene and auxin.
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Aluminium-induced inhibition of root elongation in Arabidopsis is mediated by ethylene and auxin.

机译:铝诱导的拟南芥根伸长抑制是由乙烯和生长素介导的。

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摘要

Aluminium (Al) is phytotoxic when solubilized into Alpd in acidic soils. One of the earliest and distinct symptoms of Alpd toxicity is inhibition of root elongation. To decipher the mechanism by which Alpd inhibits root elongation, the role of ethylene and auxin in Alpd-induced inhibition of root elongation in Arabidopsis thaliana was investigated using the wild type and mutants defective in ethylene signalling (etr1-3 and ein2-1) and auxin polar transport (aux1-7 and pin2). Exposure of wild-type Arabidopsis to AlCl led to a marked inhibition of root elongation, and elicited a rapid ethylene evolution and enhanced activity of the ethylene reporter EBS:GUS in root apices. Root elongation in etr1-3 and ein2-1 mutants was less inhibited by Alpd than that in wild-type plants. Ethylene synthesis inhibitors, Copo and aminoethoxyvinylglycine (AVG), and an antagonist of ethylene perception (Ag) abolished the Alpd-induced inhibition of root elongation. There was less inhibition of root elongation by Alpd in aux1-7 and pin2 mutants than in the wild type. The auxin polar transport inhibitor, naphthylphthalamic acid (NPA), substantially alleviated the Alpd-induced inhibition of root elongation. The Alpd and ethylene synthesis precursor aminocyclopropane carboxylic acid (ACC) increased auxin reporter DR5:GUS activity in roots. The Alpd-induced increase in DR5:GUS activity was reduced by AVG, while the Alpd-induced increase in EBS:GUS activity was not altered by NPA. Alpd and ACC increased transcripts of AUX1 and PIN2, and this effect was no longer observed in the presence of AVG and Copo. These findings indicate that Alpd-induced ethylene production is likely to act as a signal to alter auxin distribution in roots by disrupting AUX1- and PIN2-mediated auxin polar transport, leading to arrest of root elongation.
机译:铝(Al)在酸性土壤中溶解成Alpd时具有植物毒性。 Alpd毒性的最早且独特的症状之一是抑制根伸长。为了破译Alpd抑制根伸长的机制,使用野生型和乙烯信号传导缺陷的突变体(etr1-3和ein2-1)和突变株,研究了乙烯和生长素在拟南芥中Alpd诱导的根伸长抑制中的作用。生长素极性运输(aux1-7和pin2)。将野生型拟南芥暴露于AlCl会显着抑制根伸长,并引起快速的乙烯进化和增强的乙烯报告基因EBS:GUS在根尖的活性。与野生型植物相比,Alpd抑制etr1-3和ein2-1突变体的根伸长。乙烯合成抑制剂Copo和氨基乙氧基乙烯基甘氨酸(AVG),以及乙烯感知(Ag)的拮抗剂,废除了Alpd对根伸长的抑制作用。 Alpd在aux1-7和pin2突变体中对根伸长的抑制作用小于野生型。生长素极性转运抑制剂萘基邻苯二甲酸(NPA)基本上减轻了Alpd诱导的根伸长抑制。 Alpd和乙烯合成前体氨基环丙烷羧酸(ACC)提高了根部生长素报告基因DR5:GUS的活性。 AVG降低了Alpd诱导的DR5:GUS活性的增加,而NPA并没有改变Alpd诱导的EBS:GUS活性的增加。 Alpd和ACC增加了AUX1和PIN2的转录本,在AVG和Copo的存在下不再观察到这种效果。这些发现表明,Alpd诱导的乙烯生成很可能是通过破坏AUX1和PIN2介导的生长素极性运输来改变根中生长素分布的信号,从而导致根伸长的停止。

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