Role of hormones in the induction of iron deficiency responses in Arabidopsis roots.
Role of hormones in the induction of iron deficiency responses in Arabidopsis roots.
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DOI：
10.1104/pp.122.4.1109
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发表时间：
2000-04
期刊：
影响因子：
7.4
通讯作者：
Wolfgang Schmidt;Julia Tittel;Adam Schikora
中科院分区：
文献类型：
--
作者：
Wolfgang Schmidt;Julia Tittel;Adam Schikora
在“策略I”植物中，根生理和形态的几个变化是由缺铁引起的，尽管低铁水平转化为旨在缓解铁短缺的反应的机制在很大程度上是未知的。为了证明是否在激素浓度或敏感性的变化参与适应次优铁的可用性，我们测试了45突变体的拟南芥激素代谢和/或根毛形成缺陷的能力，以增加铁（III）螯合还原酶的活性，并启动根毛的形成和扩大。铁螯合还原酶活性染色显示，所有的突变体响应铁缺乏，这表明激素是不必要的诱导。用乙烯前体1-氨基环丙烷-1-羧酸处理野生型植物引起通常由非毛细胞占据的位置中根毛的发育，但不刺激铁还原酶活性。异位根毛也形成在-Fe根，表明乙烯的形态反应，铁缺乏的作用。根皮层细胞的超微结构分析表明，无论是铁缺乏，也没有1-氨基环丙烷-1-羧酸处理引起的拟南芥根转移细胞样改变。我们的数据表明，铁应激综合征的形态和生理成分分别调节。
In "strategy I" plants, several alterations in root physiology and morphology are induced by Fe deficiency, although the mechanisms by which low Fe levels are translated into reactions aimed at alleviating Fe shortage are largely unknown. To prove whether changes in hormone concentration or sensitivity are involved in the adaptation to suboptimal Fe availability, we tested 45 mutants of Arabidopsis defective in hormone metabolism and/or root hair formation for their ability to increase Fe(III) chelate reductase activity and to initiate the formation and enlargement of root hairs. Activity staining for ferric chelate reductase revealed that all mutants were responsive to Fe deficiency, suggesting that hormones are not necessary for the induction. Treatment of wild-type plants with the ethylene precursor 1-aminocyclopropane-1-carboxylic acid caused the development of root hairs in locations normally occupied by non-hair cells, but did not stimulate ferric reductase activity. Ectopic root hairs were also formed in -Fe roots, suggesting a role for ethylene in the morphological responses to Fe deficiency. Ultrastructural analysis of rhizodermal cells indicated that neither Fe deficiency nor 1-aminocyclopropane-1-carboxylic acid treatment caused transfer-cell-like alterations in Arabidopsis roots. Our data indicate that the morphological and physiological components of the Fe stress syndrome are regulated separately.