ArticleNature communications2025
A multiprotein regulatory module, MED16-MBR1&2, controls MED25 homeostasis during jasmonate signaling.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- SlMED25-SlPHR3-SlSPX2 module fine-tunes SlPHR3-mediated transcriptional activation of phosphate starvation response in tomato.Journal of integrative plant biology · 2026Article
- Wheat TaSPL13-2B Improves Floret Fertility and Enhances Grain Number per Spikelet Through Jasmonic Acid Signalling Pathway.Plant biotechnology journal · 2026Article
- Jasmonate Modulates Strawberry Susceptibility to Anthracnose by Activating SnRK2.1 to Regulate the WRKY50-JAZ5 Module.Plant biotechnology journal · 2026Article
- When MED16 Meets Plant Growth, Development, and Stress Response.International journal of molecular sciences · 2026Review
- The environmentally responsive plant epigenome: insights from jasmonate signaling.The New phytologist · 2026Review
- Unlocking tropical adaptation: novel flowering time genes implicate JA and ROS signaling in maize.BMC plant biology · 2026Article
- The Synergistic Effects of Jasmonic Acid and Arbuscular Mycorrhizal Fungi in Enhancing the Herbicide Resistance of an Invasive WeedMicroorganisms · 2025Article
- Molecular Decoding of Phytohormone Crosstalk: JA-Mediated Key Regulatory Nodes and Signal Integration.Plants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Mediator25 (MED25) has been ascribed as a signal-processing and -integrating center that controls jasmonate (JA)-induced and MYC2-dependent transcriptional output. A better understanding of the regulation of MED25 stability will undoubtedly advance our knowledge of the precise regulation of JA signaling-related transcriptional output. Here, we report that Arabidopsis MED16 activates JA-responsive gene expression by promoting MED25 stability. Conversely, two homologous E3 ubiquitin ligases, MED25-BINDING RING-H2 PROTEIN1 (MBR1) and MBR2, negatively regulate JA-responsive gene expression by promoting MED25 degradation. MED16 competes with MBR1&2 to bind to the von Willebrand Factor A (vWF-A) domain of MED25, thereby antagonizing the MBR1&2-mediated degradation of MED25 in vivo. In addition, we show that MED16 promotes hormone-induced interactions between MYC2 and MED25, leading to the activation of JA-responsive gene expression. Collectively, our findings reveal a multiprotein regulatory module that robustly and tightly maintains MED25 homeostasis, which determines the strength of the transcriptional output of JA signaling.
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Registered trials
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