The cleaved C-terminal domain of GmERS1-1 modulates cell cycle via GmACR1
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Ethylene signaling orchestrates plant development and stress adaptation, yet how post-translational modifications of its receptors coordinate growth regulation remains unresolved. Here, we uncover a proteolytic processing mechanism of the soybean ethylene receptor GmERS1-1 that directly gates cell cycle progression. The GmERS1-1 mutants exhibit elevated yield under field conditions, whereas overexpression suppresses growth and hypersensitizes plants to ethylene. Ethylene triggers nuclear translocation of C-terminal domain (GmERS1-1-CEND), which is indispensable for receptor function. Mechanistically, GmERS1-1-CEND scaffolds a trimeric complex with GmACR1 and GmCDK7, enforcing G2/M phase arrest, thereby decoupling cell division from canonical ethylene transcriptional responses. Strikingly, ethylene-induced cell cycle blockade during apple fruit maturation mirrors this pathway, suggesting deep conservation across angiosperms. Our work defines a receptor processing-dependent signaling axis that directly interlinks phytohormone perception with cell cycle control, proposing tunable targets (e.g., GmERS1-1 cleavage efficiency) for engineering crop architecture and productivity.
In brief
The cleaved C-terminal fragment of ethylene receptor GmERS1-1 enters into nucleus to inhibit cell cycle via interaction with GmACR1 in soybean.
Highlights
Mutating ethylene receptor GmERS1-1 significantly increases soybean yield in field.
The cleaved C-terminal fragment of GmERS1-1 enters into the nucleus induced by ethylene and independent of CTR1.
The C-terminal fragment has similar function to the full-length ethylene receptor GmERS1-1 to induce ethylene reaction in soybean and Arabidopsis .
The C-terminal fragment of GmERS1-1 interacts with soybean GmACR1 to inhibit cell division.
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The cleaved C-terminal domain of GmERS1-1 modulates cell cycle via GmACR1 https://www.biorxiv.org/content/10.64898/2026.10.07.757225v1
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The cleaved C-terminal domain of GmERS1-1 modulates cell cycle via GmACR1 https://www.biorxiv.org/content/10.64898/2026.10.07.757225v1
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