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by claude@2026-07, 2026-07-14
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The study examined how abscisic acid (ABA) signaling regulates cadmium (Cd) tolerance in Arabidopsis, focusing on the ABI5-WRKY45-LSU1 regulatory axis. Under Cd stress, ABA biosynthesis increased and ABI5 expression was upregulated; abi5-8 mutants showed increased Cd sensitivity, while ABI5 was found to directly bind an ABRE element in the WRKY45 promoter to activate WRKY45 transcription. Transcriptome analysis and validation (qRT-PCR, DUAL-LUC, and EMSA) identified LSU1 as a WRKY45 target, with WRKY45 binding a W-box in the LSU1 promoter; LSU1 overexpression enhanced Cd tolerance by increasing sulfur assimilation products (non-protein thiols, glutathione, and phytochelatins), and LSU1 acted downstream of WRKY45 but upstream of and depending on APS1 for this effect. The paper explicitly relates to endometriosis or adenomyosis; it does not discuss these conditions.
Abstract
Abscisic acid (ABA) is involved in Cd tolerance in Arabidopsis, but the underlying mechanisms are unclear. In this study, we revealed that the ABI5-WRKY45-LSU1 axis confers the tolerance of Arabidopsis to Cd stress. Under Cd stress, the biosynthesis of ABA is increased, and the expression of transcription factor ABI5 is upregulated. Accordingly, the abi5-8 mutants show increased Cd sensitivity. ABI5 directly binds the ABRE element in the WRKY45 promoter to activate its transcription. Overexpression of WRKY45 rescues the Cd-hypersensitive phenotype of the abi5-8 mutant, placing WRKY45 downstream of ABI5 . Transcriptome analyses identified LSU1 as a potential WRKY45 target. qRT-PCR, DUAL-LUC and EMSA experiments verified that WRKY45 binds the W-box cis -element in the LSU1 promoter to activate its expression. Overexpression of LSU1 enhances Cd tolerance by promoting the biosynthesis of non-protein thiols (NPT), glutathione (GSH), and phytochelatins (PC). Moreover, overexpression of LSU1 suppresses Cd sensitivity in the wrky45 mutant, confirming LSU1 acts downstream of WRKY45 . On the other hand, we found that ATP sulfurylase 1 (APS1) interacts with LSU1 based in vitro and in vivo evidences. LSU1 stabilizes APS1, slows its degradation, and enhances APS1 activity, thus leading to increased NPT, GSH, and PC accumulation and improved Cd detoxification. Notably, overexpressing LSU1 did not rescue the Cd sensitivity of the aps1-1 mutant, indicating that LSU1 acts upstream of and depends on APS1 . In short, we demonstrated a novel ABI5-WRKY45-LSU1 axis that regulates Cd tolerance through sulfur assimilation and phytochelatin synthesis. Highlights Cadmium stress triggers ABA biosynthesis and ABI5 expression; ABI5 directly binds to ABRE motifs in the WRKY45 promoter and activates its transcription. WRKY45 transcriptionally activates LSU1, and LSU1 interacts with APS1 to stabilize it and elevate ATP sulfurylase activity, acting in an APS1-dependent manner. The ABI5–WRKY45–LSU1 module enhances Arabidopsis Cd tolerance by boosting sulfur assimilation and GSH/PC-mediated Cd detoxification, rather than reducing Cd uptake.
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Abstract
Abscisic acid (ABA) is involved in Cd tolerance in Arabidopsis, but the underlying mechanisms are unclear. In this study, we revealed that the ABI5-WRKY45-LSU1 axis confers the tolerance of Arabidopsis to Cd stress. Under Cd stress, the biosynthesis of ABA is increased, and the expression of transcription factor ABI5 is upregulated. Accordingly, the abi5-8 mutants show increased Cd sensitivity. ABI5 directly binds the ABRE element in the WRKY45 promoter to activate its transcription. Overexpression of WRKY45 rescues the Cd-hypersensitive phenotype of the abi5-8 mutant, placing WRKY45 downstream of ABI5. Transcriptome analyses identified LSU1 as a potential WRKY45 target. qRT-PCR, DUAL-LUC and EMSA experiments verified that WRKY45 binds the W-box cis-element in the LSU1 promoter to activate its expression. Overexpression of LSU1 enhances Cd tolerance by promoting the biosynthesis of non-protein thiols (NPT), glutathione (GSH), and phytochelatins (PC). Moreover, overexpression of LSU1 suppresses Cd sensitivity in the wrky45 mutant, confirming LSU1 acts downstream of WRKY45. On the other hand, we found that ATP sulfurylase 1 (APS1) interacts with LSU1 based in vitro and in vivo evidences. LSU1 stabilizes APS1, slows its degradation, and enhances APS1 activity, thus leading to increased NPT, GSH, and PC accumulation and improved Cd detoxification. Notably, overexpressing LSU1 did not rescue the Cd sensitivity of the aps1-1 mutant, indicating that LSU1 acts upstream of and depends on APS1. In short, we demonstrated a novel ABI5-WRKY45-LSU1 axis that regulates Cd tolerance through sulfur assimilation and phytochelatin synthesis.
Highlights
Cadmium stress triggers ABA biosynthesis and ABI5 expression; ABI5 directly binds to ABRE motifs in the WRKY45 promoter and activates its transcription.
WRKY45 transcriptionally activates LSU1, and LSU1 interacts with APS1 to stabilize it and elevate ATP sulfurylase activity, acting in an APS1-dependent manner.
The ABI5–WRKY45–LSU1 module enhances Arabidopsis Cd tolerance by boosting sulfur assimilation and GSH/PC-mediated Cd detoxification, rather than reducing Cd uptake.
Competing Interest Statement
The authors have declared no competing interest.
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