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<p>Maintaining root meristem activity under environmental stress is critical for plant growth and survival. The RNA-binding protein FLOWERING CONTROL LOCUS A (FCA) is well known for its role in floral transition and RNA metabolism, but its function in root development under stress conditions remains uncharacterized. Here, we demonstrate that FCA is essential for maintaining root thermomorphogenesis through its interaction with SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a central transcription factor in the DNA damage response. At elevated ambient temperatures, <i>fca</i> mutants display severe defects in primary root growth with compromised root meristem activity. FCA physically interacts with SOG1, and loss-of-function <i>fca</i> mutation led to highly induced expression of SOG1 target genes, including those involved in cell cycle regulation. Consistent with this, the <i>fca sog1</i> double mutant exhibited a notable rescue of the root growth defects of <i>fca</i> mutant at high temperatures, indicating the FCA function in root thermomorphogenesis is largely dependent on SOG1 activity. Collectively, our findings reveal a previously unrecognized role of FCA in sustaining root meristem activity at high ambient temperatures by attenuating SOG1-mediated stress responses.</p>

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FCA Contributes to Root Thermomorphogenesis by Attenuating SOG1-Mediated Stress Signaling in Arabidopsis

  • 期刊论文

  • 发表日期：

    2025年11月6日

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

摘要

Maintaining root meristem activity under environmental stress is critical for plant growth and survival. The RNA-binding protein FLOWERING CONTROL LOCUS A (FCA) is well known for its role in floral transition and RNA metabolism, but its function in root development under stress conditions remains uncharacterized. Here, we demonstrate that FCA is essential for maintaining root thermomorphogenesis through its interaction with SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a central transcription factor in the DNA damage response. At elevated ambient temperatures, fca mutants display severe defects in primary root growth with compromised root meristem activity. FCA physically interacts with SOG1, and loss-of-function fca mutation led to highly induced expression of SOG1 target genes, including those involved in cell cycle regulation. Consistent with this, the fca sog1 double mutant exhibited a notable rescue of the root growth defects of fca mutant at high temperatures, indicating the FCA function in root thermomorphogenesis is largely dependent on SOG1 activity. Collectively, our findings reveal a previously unrecognized role of FCA in sustaining root meristem activity at high ambient temperatures by attenuating SOG1-mediated stress responses.