Nitric Oxide Acts Downstream of Auxin to Trigger Root Ferric-Chelate Reductase Activity in Response to Iron Deficiency in Arabidopsis
Nitric Oxide Acts Downstream of Auxin to Trigger Root Ferric-Chelate Reductase Activity in Response to Iron Deficiency in Arabidopsis
复制标题
一氧化氮作用于生长素下游，触发根部铁螯合物还原酶活性，以应对拟南芥缺铁
DOI：
10.1104/pp.110.161109
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发表时间：
2010-10-01
期刊：
影响因子：
7.4
通讯作者：
Zheng, Shao Jian
中科院分区：
文献类型：
--
作者：
Chen, Wei Wei;Yang, Jian Li;Zheng, Shao Jian
为了应对铁（Fe）缺乏，双子叶植物采用基于还原的机制，通过诱导根质膜上的铁螯合物还原酶（FCR）来增强Fe的吸收。然而，导致FCR诱导的信号通路仍然不清楚。在这里，我们发现，铁缺乏诱导的生长素和一氧化氮（NO）水平在野生型拟南芥（拟南芥）的增加伴随着上调根FCR活性和表达的基本螺旋-环-螺旋转录因子（FIT）和铁还原氧化酶2（FRO 2）基因。这是进一步刺激应用外源性生长素（α-萘乙酸）或NO供体（S-亚硝基谷胱甘肽[GSNO]），但抑制极性生长素运输抑制与α-萘基邻苯二甲酰胺酸或NO清除2-（4-羧基苯基）-4，4，5，5-四甲基咪唑啉-1-氧基-3-氧化物，钨酸盐，或N-ω-硝基-L-精氨酸甲酯盐酸盐。而生长素高产突变体丝兰在缺铁胁迫下，根系FCR活性、NO含量以及FIT和FRO 2基因表达量均高于对照，但2-（4-羧基苯基）-4，4，5，5-四甲基咪唑啉-1-氧-3-氧化物处理显著抑制了FIT和FRO 2基因表达。相反的反应，观察到在一个向基生长素运输受损的突变体aux 1 -7，这是轻微抢救外源GSNO的应用。此外，缺铁或α-萘乙酸的应用未能诱导缺铁的反应noa 1和拟南芥2，两个突变体与减少NO合成，但根FCR活性在这两个突变体可以显着提高GSNO。不能诱导NO爆发和FCR活性进一步验证了在双突变体丝兰noa 1与升高的生长素生产和减少NO积累。因此，我们提出了一个新的信号通路，NO的行为下游的生长素激活根FCR活性铁缺乏下在拟南芥。
In response to iron (Fe) deficiency, dicots employ a reduction-based mechanism by inducing ferric-chelate reductase (FCR) at the root plasma membrane to enhance Fe uptake. However, the signal pathway leading to FCR induction is still unclear. Here, we found that the Fe-deficiency-induced increase of auxin and nitric oxide (NO) levels in wild-type Arabidopsis (Arabidopsis thaliana) was accompanied by up-regulation of root FCR activity and the expression of the basic helix-loop-helix transcription factor (FIT) and the ferric reduction oxidase 2 (FRO2) genes. This was further stimulated by application of exogenous auxin (a-naphthaleneacetic acid) or NO donor (S-nitrosoglutathione [GSNO]), but suppressed by either polar auxin transport inhibition with alpha-naphthylphthalamic acid or NO scavenging with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, tungstate, or N-omega-nitro-L-arginine methyl ester hydrochloride. On the other hand, the root FCR activity, NO level, and gene expression of FIT and FRO2 were higher in auxin-overproducing mutant yucca under Fe deficiency, which were sharply restrained by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide treatment. The opposite response was observed in a basipetal auxin transport impaired mutant aux1-7, which was slightly rescued by exogenous GSNO application. Furthermore, Fe deficiency or alpha-naphthaleneacetic acid application failed to induce Fe-deficiency responses in noa1 and nial nia2, two mutants with reduced NO synthesis, but root FCR activities in both mutants could be significantly elevated by GSNO. The inability to induce NO burst and FCR activity was further verified in a double mutant yucca noa1 with elevated auxin production and reduced NO accumulation. Therefore, we presented a novel signaling pathway where NO acts downstream of auxin to activate root FCR activity under Fe deficiency in Arabidopsis.