<p>Cold stress restricts root growth by disrupting stem cell activity in plants. C-REPEAT BINDING FACTORs (CBFs) are central regulators of cold signalling and also modulate root stem cell activity. While the receptor-like cytoplasmic kinase CRPK1 promotes CBF destabilization under cold stress, its regulatory partner remains unclear. Here we identify KINASE ON THE INSIDE (KOIN), a plasma-membrane-localized receptor-like kinase, as a crucial interactor of CRPK1. The loss of either <i>KOIN</i> or <i>CRPK1</i> results in cold-insensitive root phenotypes, characterized by sustained primary root elongation and enhanced cortex cell proliferation via the 14-3-3–CBF3–SHR pathway. Under cold stress, KOIN undergoes endocytosis and is recycled back to the plasma membrane in a CRPK1-dependent manner. Although catalytically inactive, KOIN modulates CRPK1 protein levels and phosphorylation through a non-catalytic mechanism. These findings uncover a membrane-to-nucleus signalling module that integrates receptor trafficking with intracellular kinase activity to mediate cold-induced root growth inhibition in <i>Arabidopsis</i>.</p>

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A receptor–kinase cascade confers cold-induced root growth inhibition in Arabidopsis

  • Xiuyue Zhang,
  • Minze Li,
  • Xiaoyan Zhang,
  • Rong Zeng,
  • Yue Peng,
  • Yiting Shi,
  • Xiangfeng Wang,
  • Wenkun Zhou,
  • Zhizhong Gong,
  • Shuhua Yang

摘要

Cold stress restricts root growth by disrupting stem cell activity in plants. C-REPEAT BINDING FACTORs (CBFs) are central regulators of cold signalling and also modulate root stem cell activity. While the receptor-like cytoplasmic kinase CRPK1 promotes CBF destabilization under cold stress, its regulatory partner remains unclear. Here we identify KINASE ON THE INSIDE (KOIN), a plasma-membrane-localized receptor-like kinase, as a crucial interactor of CRPK1. The loss of either KOIN or CRPK1 results in cold-insensitive root phenotypes, characterized by sustained primary root elongation and enhanced cortex cell proliferation via the 14-3-3–CBF3–SHR pathway. Under cold stress, KOIN undergoes endocytosis and is recycled back to the plasma membrane in a CRPK1-dependent manner. Although catalytically inactive, KOIN modulates CRPK1 protein levels and phosphorylation through a non-catalytic mechanism. These findings uncover a membrane-to-nucleus signalling module that integrates receptor trafficking with intracellular kinase activity to mediate cold-induced root growth inhibition in Arabidopsis.