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<p>In <i>Arabidopsis</i>, the two MADS-box transcription factors FLOWERING LOCUS M (FLM) and SHORT VEGETATIVE PHASE (SVP) form a repressor complex that controls temperature-responsive flowering. Alternative splicing of <i>FLM</i> generates two predominant isoforms, FLM-β and FLM-δ. FLM-β facilitates SVP nuclear accumulation at low temperatures, whereas FLM-δ cause cytoplasmic retention and ubiquitin-mediated degradation of SVP at high temperatures. Here, we show that the microRNA172 (miR172) target transcription factor TARGET OF EAT1 (TOE1) is also incorporated into the FLM–SVP repressor complex. TOE1 physically interacts with FLM, but not directly with SVP, and FLM is required for the TOE1–SVP interaction. Overexpression of <i>TOE1</i> failed to delay flowering in <i>svp-32</i> or <i>flm-3</i> mutant backgrounds, indicating that TOE1 function depends on both SVP and FLM. Notably, the interactions of TOE1 with SVP and FLM were stronger at low temperatures but attenuated at high temperatures, supporting that the TOE1–FLM–SVP repressor complex formation is temperature-regulated. Together, our findings reveal that TOE1-mediated repression of flowering is dependent on the FLM–SVP complex, expanding the current model of temperature-responsive flowering by linking the miR172–TOE1 signaling pathway to the FLM–SVP regulatory module.</p>

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TOE1 Interacts with FLM and SVP to Repress Flowering in Arabidopsis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月14日

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  • Jae-Eun Woo,
  • Yun-Young Choi,
  • Jihyeon Park,
  • Jae-Hoon Jung

摘要

In Arabidopsis, the two MADS-box transcription factors FLOWERING LOCUS M (FLM) and SHORT VEGETATIVE PHASE (SVP) form a repressor complex that controls temperature-responsive flowering. Alternative splicing of FLM generates two predominant isoforms, FLM-β and FLM-δ. FLM-β facilitates SVP nuclear accumulation at low temperatures, whereas FLM-δ cause cytoplasmic retention and ubiquitin-mediated degradation of SVP at high temperatures. Here, we show that the microRNA172 (miR172) target transcription factor TARGET OF EAT1 (TOE1) is also incorporated into the FLM–SVP repressor complex. TOE1 physically interacts with FLM, but not directly with SVP, and FLM is required for the TOE1–SVP interaction. Overexpression of TOE1 failed to delay flowering in svp-32 or flm-3 mutant backgrounds, indicating that TOE1 function depends on both SVP and FLM. Notably, the interactions of TOE1 with SVP and FLM were stronger at low temperatures but attenuated at high temperatures, supporting that the TOE1–FLM–SVP repressor complex formation is temperature-regulated. Together, our findings reveal that TOE1-mediated repression of flowering is dependent on the FLM–SVP complex, expanding the current model of temperature-responsive flowering by linking the miR172–TOE1 signaling pathway to the FLM–SVP regulatory module.