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<p>Sucrose (Suc) must be hydrolyzed by invertase into glucose (Glc) and fructose (Fru) to support plant growth. Prior studies in <i>Arabidopsis</i> established a regulatory circuit in which Glc signaling—via the sensor HXK1—destabilizes the transcription factor EIN3, which directly represses PAP1 and activates PIP5K9. PAP1 activates <i>CINV1</i> expression, while PIP5K9 protein inhibits CINV1 activity. Cleavage of Suc by CINV1 releases Glc, thereby closing a feedback loop that modulates root growth. However, the specificity of this loop for root growth and the potential role of auxin remained unknown. Here, we demonstrate that glucose specifically enhances root growth and development through increased cytosolic invertase activity, and that auxin is not a primary contributor to this process. Furthermore, we show that the feedback regulation operates independently of general nutrient effects and is uniquely sensitive to cellular Glc levels. Our findings establish the CINV1–Glc–HXK1–EIN3–PAP1/PIP5K9 module as a dedicated root growth regulator and discuss its broader physiological implications for carbon allocation and developmental plasticity.</p>

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A glucose-dependent signaling loop regulates root growth

  • 期刊论文

  • 发表日期：

    2025年9月26日

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  • Jiang-Ping Song,
  • Hua Xu

摘要

Sucrose (Suc) must be hydrolyzed by invertase into glucose (Glc) and fructose (Fru) to support plant growth. Prior studies in Arabidopsis established a regulatory circuit in which Glc signaling—via the sensor HXK1—destabilizes the transcription factor EIN3, which directly represses PAP1 and activates PIP5K9. PAP1 activates CINV1 expression, while PIP5K9 protein inhibits CINV1 activity. Cleavage of Suc by CINV1 releases Glc, thereby closing a feedback loop that modulates root growth. However, the specificity of this loop for root growth and the potential role of auxin remained unknown. Here, we demonstrate that glucose specifically enhances root growth and development through increased cytosolic invertase activity, and that auxin is not a primary contributor to this process. Furthermore, we show that the feedback regulation operates independently of general nutrient effects and is uniquely sensitive to cellular Glc levels. Our findings establish the CINV1–Glc–HXK1–EIN3–PAP1/PIP5K9 module as a dedicated root growth regulator and discuss its broader physiological implications for carbon allocation and developmental plasticity.