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<p>Functional divergence of gene homologs enables species to evolve unique physiological processes, such as nitrogen fixation of nodules in legumes. Nodulation is initiated via rhizobia-induced reactivation of root cortical cells into stem cells, yet the molecular mechanism underlying this process has remained elusive. There are eight florigen homologs in the soybean genome, including <i>GmFT2a</i> and <i>GmFT5a</i>, which are produced in leaves and possibly translocated to roots to promote nodulation. Here, we report the identification of a distinct florigen homolog, <i>GmFT5b</i>, and its partner <i>GmFDL23</i>, both of which are locally upregulated in the root cortex upon rhizobia infection. This <i>GmFT5b-GmFDL23</i> module directly suppresses <i>GmCLV3-1</i> expression in the root cortex, thereby alleviating its repression of the stem cell regulator <i>GmWUS1</i>, which further drives cortical cell reprogramming into nodule stem cells. Our findings delineate a florigen-mediated pathway that spatiotemporally controls stem cells in cortex to drive nodule formation.</p>

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A rhizobium-induced FT-FD module locally activates nodule stem cell gene to promote nodulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月23日

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  • Huiyu Sun,
  • Xiaomei Zhang,
  • Chao Ma,
  • Penghui Huang,
  • Qi Sun,
  • Guolong Yu,
  • Limin Liu,
  • Mingyang Lu,
  • Lu Han,
  • Kexin Qu,
  • Xianzhong Feng,
  • Yuchen Miao,
  • Qingshan Chen,
  • Jingjuan Yu,
  • Dawei Xin,
  • Yong-Fu Fu

摘要

Functional divergence of gene homologs enables species to evolve unique physiological processes, such as nitrogen fixation of nodules in legumes. Nodulation is initiated via rhizobia-induced reactivation of root cortical cells into stem cells, yet the molecular mechanism underlying this process has remained elusive. There are eight florigen homologs in the soybean genome, including GmFT2a and GmFT5a, which are produced in leaves and possibly translocated to roots to promote nodulation. Here, we report the identification of a distinct florigen homolog, GmFT5b, and its partner GmFDL23, both of which are locally upregulated in the root cortex upon rhizobia infection. This GmFT5b-GmFDL23 module directly suppresses GmCLV3-1 expression in the root cortex, thereby alleviating its repression of the stem cell regulator GmWUS1, which further drives cortical cell reprogramming into nodule stem cells. Our findings delineate a florigen-mediated pathway that spatiotemporally controls stem cells in cortex to drive nodule formation.