Complex control of seed germination timing by ERF 50 involves RGL 2 antagonism and negative feedback regulation of DOG1

• Published in: The New phytologist 2024-06, Vol.242 (5), p.2026-2042
• Main Authors: Carrera‐Castaño, Gerardo, Mira, Sara, Fañanás‐Pueyo, Iris, Sánchez‐Montesino, Rocío, Contreras, Ángela, Weiste, Christoph, Dröge‐Laser, Wolfgang, Gómez, Luis, Oñate‐Sánchez, Luis
• Format: Article
• Language: English
• ISSN: 0028-646X; 1469-8137
• DOI: 10.1111/nph.19681

Seed dormancy governs germination timing, with both evolutionary and applied consequences. Despite extensive studies on the hormonal and genetic control of these processes, molecular mechanisms directly linking dormancy and germination remain poorly understood. By screening a collection of lines overexpressing Arabidopsis transcription factors, we identified ERF50 as a key gene to control dormancy and germination. To study its regulation, we measured seed‐related physiological parameters in loss‐of‐function mutants and carried out transactivation, protein interaction and ChIP‐PCR analyses. We found direct ERF50‐mediated repression of DOG1 and activation of EXPA2 transcription, which results in enhanced seed germination. Although ERF50 expression is increased by DOG1 in dormant seeds, ERF50 germination‐promoting activity is blocked by RGL2. The physiological, genetic and molecular evidence gathered here supports that ERF50 controls germination timing by regulating DOG1 levels to leverage its role as enhancer of seed germination, via RGL2 antagonism on EXPA2 expression. Our results highlight the central role of ERF50 as a feedback regulator to couple and fine‐tune seed dormancy and germination.