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Plant Cell. 2017 Jan;29(1):54-69. doi: 10.1105/tpc.16.00623. Epub 2016 Dec 23.

WIND1 Promotes Shoot Regeneration through Transcriptional Activation of ENHANCER OF SHOOT REGENERATION1 in Arabidopsis.

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RIKEN Center for Sustainable Resource Science, Yokohama 230-0045, Japan.
Center for Applied Plant Sciences and Department of Molecular Genetics, The Ohio State University, Columbus, Ohio 43210.
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma 630-0192, Japan.
National Institute of Advanced Industrial Science and Technology, Tsukuba 305-8562, Japan.
Graduate School of Science and Engineering, Saitama University, Saitama 338-8570, Japan.
RIKEN Center for Sustainable Resource Science, Yokohama 230-0045, Japan


Many plant species display remarkable developmental plasticity and regenerate new organs after injury. Local signals produced by wounding are thought to trigger organ regeneration but molecular mechanisms underlying this control remain largely unknown. We previously identified an AP2/ERF transcription factor WOUND INDUCED DEDIFFERENTIATION1 (WIND1) as a central regulator of wound-induced cellular reprogramming in plants. In this study, we demonstrate that WIND1 promotes callus formation and shoot regeneration by upregulating the expression of the ENHANCER OF SHOOT REGENERATION1 (ESR1) gene, which encodes another AP2/ERF transcription factor in Arabidopsis thaliana The esr1 mutants are defective in callus formation and shoot regeneration; conversely, its overexpression promotes both of these processes, indicating that ESR1 functions as a critical driver of cellular reprogramming. Our data show that WIND1 directly binds the vascular system-specific and wound-responsive cis-element-like motifs within the ESR1 promoter and activates its expression. The expression of ESR1 is strongly reduced in WIND1-SRDX dominant repressors, and ectopic overexpression of ESR1 bypasses defects in callus formation and shoot regeneration in WIND1-SRDX plants, supporting the notion that ESR1 acts downstream of WIND1. Together, our findings uncover a key molecular pathway that links wound signaling to shoot regeneration in plants.

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