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A NAC‐type transcription factor confers aluminium resistance by regulating cell wall‐associated receptor kinase 1 and cell wall pectin
Author(s) -
Lou He Qiang,
Fan Wei,
Jin Jian Feng,
Xu Jia Meng,
Chen Wei Wei,
Yang Jian Li,
Zheng Shao Jian
Publication year - 2020
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/pce.13676
Subject(s) - arabidopsis , transcription factor , biology , microbiology and biotechnology , cell wall , gene , gene expression , transcriptional regulation , kinase , biochemistry , mutant
Transcriptional regulation is important for plants to respond to toxic effects of aluminium (Al). However, our current knowledge to these events is confined to a few transcription factors. Here, we functionally characterized a rice bean ( Vigna umbellata ) NAC‐type transcription factor, VuNAR1, in terms of Al stress response. We demonstrated that rice bean VuNAR1 is a nuclear‐localized transcriptional activator, whose expression was specifically upregulated by Al in roots but not in shoot. VuNAR1 overexpressing Arabidopsis plants exhibit improved Al resistance via Al exclusion. However, VuNAR1‐mediated Al exclusion is independent of the function of known Al‐resistant genes. Comparative transcriptomic analysis revealed that VuNAR1 specifically regulates the expression of genes associated with protein phosphorylation and cell wall modification in Arabidopsis . Transient expression assay demonstrated the direct transcriptional activation of cell wall‐associated receptor kinase 1 ( WAK1 ) by VuNAR1. Moreover, yeast one‐hybrid assays and MEME motif searches identified a new VuNAR1‐specific binding motif in the promoter of WAK1 . Compared with wild‐type Arabidopsis plants, VuNAR1 overexpressing plants have higher WAK1 expression and less pectin content. Taken together, our results suggest that VuNAR1 regulates Al resistance by regulating cell wall pectin metabolism via directly binding to the promoter of WAK1 and induce its expression.

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