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<p>The SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) transcription factor plays a pivotal role in maintaining cellular ion balance and governing aluminum tolerance in plants. Abscisic acid (ABA) participates in aluminum tolerance by inducing the expression of several genes that are STOP1 targets. However, the interplay between ABA signaling and STOP1-mediated gene expression remains poorly understood. The F-box protein RAE1, an SCF-type E3 ligase component, recognizes STOP1 and controls its ubiquitination and degradation. This study revealed that exogenous ABA supplementation reduced STOP1 levels by promoting the expression of <i>RAE1</i>. Notably, both <i>RAE1</i> loss-of-function mutants and <i>STOP1</i> overexpressing lines showed enhanced sensitivity to exogenous ABA treatment, which correlated with early stage post-transcriptional upregulation of ABSCISIC ACID INSENSITIVE5 (ABI5). Our observations suggest that RAE1 operates as an ABA-responsive factor, exerting control over STOP1 homeostasis to regulate ABA responses in Arabidopsis. Interestingly, the <i>STOP1</i> dysfunctional alleles exhibit ABA sensitivity despite a reduction in ABI5, with similar expression levels of ABA-responsive genes, except for the ABI5 repressor MFT, compared to the <i>rae1</i> and STOP1 overexpression lines. This may suggest a bidirectional role of STOP1 in ABA sensitivity and highlights the critical importance of maintaining STOP1 homeostasis to balance growth and stress tolerance.</p>

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The RAE1-STOP1 module regulates ABA sensitivity in early seedlings of Arabidopsis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月13日

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  • Yuqing Zhang,
  • Min Huang,
  • Yinyin Liu,
  • Mengmeng Yang,
  • Yuqi Hou,
  • Chao-Feng Huang,
  • Ning Ning Wang,
  • Lei Li

摘要

The SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) transcription factor plays a pivotal role in maintaining cellular ion balance and governing aluminum tolerance in plants. Abscisic acid (ABA) participates in aluminum tolerance by inducing the expression of several genes that are STOP1 targets. However, the interplay between ABA signaling and STOP1-mediated gene expression remains poorly understood. The F-box protein RAE1, an SCF-type E3 ligase component, recognizes STOP1 and controls its ubiquitination and degradation. This study revealed that exogenous ABA supplementation reduced STOP1 levels by promoting the expression of RAE1. Notably, both RAE1 loss-of-function mutants and STOP1 overexpressing lines showed enhanced sensitivity to exogenous ABA treatment, which correlated with early stage post-transcriptional upregulation of ABSCISIC ACID INSENSITIVE5 (ABI5). Our observations suggest that RAE1 operates as an ABA-responsive factor, exerting control over STOP1 homeostasis to regulate ABA responses in Arabidopsis. Interestingly, the STOP1 dysfunctional alleles exhibit ABA sensitivity despite a reduction in ABI5, with similar expression levels of ABA-responsive genes, except for the ABI5 repressor MFT, compared to the rae1 and STOP1 overexpression lines. This may suggest a bidirectional role of STOP1 in ABA sensitivity and highlights the critical importance of maintaining STOP1 homeostasis to balance growth and stress tolerance.