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<p>Plants have the remarkable ability to regenerate whole organisms through the formation of pluripotent cell masses from somatic cells. Cellular programs leading to fate change resemble lateral root (LR) formation and are chiefly regulated by auxin. Brassinosteroid signaling also plays an important role in LR formation, but little is known about the direct link between auxin and brassinosteroid components, such as BZR1 and BES1, in pluripotency acquisition. Here we show that gain-of-function mutants <i>bzr1-D</i> and <i>bes1-D</i> exhibit altered callus formation, yet disruption of these transcription factors does not cause major changes to callus formation or de novo organogenesis. Moreover, our data reveal that BZR1 displays enhanced expression in callus tissue and directly binds to the promoters of <i>ARF7</i> and <i>ARF19</i>, two master pluripotency regulators, leading to their enhanced transcription. Remarkably, callus formation is abrogated in <i>bzr1-D</i> upon disruption of these <i>ARF</i>s, emphasizing that the callus formation via BZR1 depends on these auxin signaling components. In conclusion, we depict a link between, ARF7, ARF19, and BZR1 in promoting pluripotency acquisition, portraying BZR1 as a major supporting factor in callus formation.</p>

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BZR1 promotes pluripotency acquisition and callus development through direct regulation of ARF7 and ARF19

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月26日

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  • Thomas Ammitsøe,
  • Elise Ebstrup,
  • Noel Blanco-Touriñán,
  • Julie Hansen,
  • Christian S Hardtke,
  • Morten Petersen,
  • Eleazar Rodriguez

摘要

Plants have the remarkable ability to regenerate whole organisms through the formation of pluripotent cell masses from somatic cells. Cellular programs leading to fate change resemble lateral root (LR) formation and are chiefly regulated by auxin. Brassinosteroid signaling also plays an important role in LR formation, but little is known about the direct link between auxin and brassinosteroid components, such as BZR1 and BES1, in pluripotency acquisition. Here we show that gain-of-function mutants bzr1-D and bes1-D exhibit altered callus formation, yet disruption of these transcription factors does not cause major changes to callus formation or de novo organogenesis. Moreover, our data reveal that BZR1 displays enhanced expression in callus tissue and directly binds to the promoters of ARF7 and ARF19, two master pluripotency regulators, leading to their enhanced transcription. Remarkably, callus formation is abrogated in bzr1-D upon disruption of these ARFs, emphasizing that the callus formation via BZR1 depends on these auxin signaling components. In conclusion, we depict a link between, ARF7, ARF19, and BZR1 in promoting pluripotency acquisition, portraying BZR1 as a major supporting factor in callus formation.