Journal
PLANT PHYSIOLOGY
Volume 185, Issue 3, Pages 1166-1181Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiaa072
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Funding
- National Key Research and Development Program of China [2019YFD1000300]
- Basic Research Program of Shandong [ZR2018ZC08N1]
- Ministry of Agriculture-Chinese [2016ZX08009003-001-006]
- Tai-Shan Scholar Program from the Shandong Provincial Government [tsqn20161021, tsxk20150901]
- National Basic Research Program of China [2015CB942900]
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The research demonstrates that arsenate inhibits primary root elongation by regulating the transcription of local auxin biosynthesis genes in Arabidopsis root tips. Furthermore, arsenate activates cytokinin signaling and stabilizes ARR1 protein to promote the transcription of ASA1 and ASB1 genes.
Interactions between plant hormones and environmental signals are important for the maintenance of root growth plasticity under ever-changing environmental conditions. Here, we demonstrate that arsenate (As-V), the most prevalent form of arsenic (As) in nature, restrains elongation of the primary root through transcriptional regulation of local auxin biosynthesis genes in the root tips of Arabidopsis (Arabidopsis thaliana) plants. The ANTHRANILATE SYNTHASE ALPHA SUBUNIT 1 (ASA1) and BETA SUBUNIT 1 (ASB1) genes encode enzymes that catalyze the conversion of chorismate to anthranilate (ANT) via the tryptophan-dependent auxin biosynthesis pathway. Our results showed that As-V upregulates ASA1 and ASB1 expression in root tips, and ASA1- and ASB1-mediated auxin biosynthesis is involved in As-V-induced root growth inhibition. Further investigation confirmed that As-V activates cytokinin signaling by stabilizing the type-B ARABIDOPSIS RESPONSE REGULATOR1 (ARR1) protein, which directly promotes the transcription of ASA1 and ASB1 genes by binding to their promoters. Genetic analysis revealed that ASA1 and ASB1 are epistatic to ARR1 in the As-V-induced inhibition of primary root elongation. Overall, the results of this study illustrate a molecular framework that explains As-V-induced root growth inhibition via crosstalk between two major plant growth regulators, auxin and cytokinin.
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