4.7 Article

Involvement of endogenous salicylic acid in iron-deficiency responses in Arabidopsis

期刊

JOURNAL OF EXPERIMENTAL BOTANY
卷 67, 期 14, 页码 4179-4193

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jxb/erw196

关键词

Fe deficiency; hormones; nutrients; RNA sequencing; salicylic acid; transcriptome analysis

资金

  1. National Natural Science Foundation of China [31401935]
  2. Zhejiang Provincial Natural Science Foundation of China [LQ14C060001, LQ14C020002]

向作者/读者索取更多资源

Salicylic acid is involved in iron-deficiency responses, while PAD4 regulates soluble Fe concentrations in Arabidopsis. Fe acquisition may be under the control of a complex interplay of hormones.Several phytohormones have been demonstrated to be involved in iron (Fe) homeostasis. We took advantage of a salicylic acid (SA) biosynthesis defective mutant phytoalexin deficient 4 (pad4: T-DNA Salk_089936) to explore the possible effects of endogenous SA on the morphological and physiological responses to Fe deprivation. The morphological and physiological analysis was carried out between Col-0 and the pad4 mutant. Under an Fe-deficiency treatment, Col-0 showed more severe leaf chlorosis and root growth inhibition compared with the pad4 mutant. The soluble Fe concentrations were significantly higher in pad4 than in Col-0 under the Fe-deficiency treatment. Fe deficiency significantly induced SA accumulation in Col-0 and the loss-of-function of PAD4 blocked this process. The requirement of endogenous SA accumulation for Fe-deficiency responses was confirmed using a series of SA biosynthetic mutants and transgenic lines. Furthermore, a comparative RNA sequencing analysis of the whole seedling transcriptomes between Col-0 and the pad4 mutant was also performed. Based on the transcriptome data, the expression levels of many auxin- and ethylene-response genes were altered in pad4 compared with Col-0. Fe deficiency increases SA contents which elevates auxin and ethylene signalling, thereby activating Fe translocation via the bHLH38/39-mediated transcriptional regulation of downstream Fe genes.

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