WIND1 promotes shoot regeneration through transcriptional activation of ENHANCER OF SHOOT REGENERATION1 in arabidopsis

Akira Iwase, Hirofumi Harashima, Momoko Ikeuchi, Bart Rymen, Mariko Ohnuma, Shinichiro Komaki, Kengo Morohashi, Tetsuya Kurata, Masaru Nakata, Masaru Ohme-Takagi, Erich Grotewold, Keiko Sugimoto

    Research output: Contribution to journalArticlepeer-review

    84 Citations (Scopus)


    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.

    Original languageEnglish
    Pages (from-to)54-69
    Number of pages16
    JournalPlant Cell
    Issue number1
    Publication statusPublished - 2017 Jan

    ASJC Scopus subject areas

    • Plant Science
    • Cell Biology


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