# Direct receptor competition gates RGL2 proteolysis for seed germination timing in Arabidopsis

## TL;DR

The paper explains how plant seeds decide when to germinate by showing how two hormones, ABA and GA, compete to control a key protein called RGL2.

## Contribution

The study reveals a new mechanism where ABA and GA receptors directly compete for RGL2, controlling its degradation and germination timing.

## Key findings

- ABA receptors (PYLs) stabilize RGL2 by binding to it and sequestering DWA1.
- GA receptors (GID1s) outcompete PYLs, allowing DWA1 to degrade RGL2.
- This competition is regulated by ABA and GA concentrations, influencing germination timing.

## Abstract

Seed germination is orchestrated by antagonistic gibberellin (GA) and abscisic acid (ABA) signals converging on the master germination repressor RGL2. Here, we unveil a receptor-competition paradigm where ABA receptors (PYLs) stabilize RGL2, both through direct physical interaction and through functional sequestration of DWA1, the CUL4–DDB1 E3 ligase substrate adapter mediating RGL2 ubiquitination. GA receptors (GID1s) counteract this stabilization by competitively displacing PYLs from RGL2, leveraging their superior binding capacity to license DWA1-mediated degradation. Crucially, this competition is defined by the concentration of abscisic acid and gibberellin as they regulate PYL and GID1 expression. Genetic epistasis confirms that PYLs act upstream of DWA1, competing directly with GID1 at RGL2. This receptor-occupied switch converts environmental fluctuations into proteolytic decisions: transient stress imposes a reversible “pause state” through PYL dominance, while sustained GA biosynthesis permits germination via GID1-mediated degradation. Our work establishes direct receptor competition as a complementary layer to hormone crosstalk, providing a universal framework for signal-driven developmental transitions.

Plant germination timing depends on concentrations of gibberellin (GA) and abscisic acid (ABA), but the mechanisms that coordinate these signalling inputs are poorly understood. Here, GA and ABA receptors are found to directly compete for binding to the master inhibitor of germination, RGL2, and exert opposite effects on its stability.

ABA receptors (PYLs) directly bind RGL2 and block degradation of this master germination repressor.Gibberellin receptors (GID1s) outcompete PYLs for RGL2 occupancy through superior binding affinity.DWA1, a CUL4-DDB1 substrate receptor, functions as an executor of GA signaling by mediating RGL2 ubiquitination and degradation.PYLs sequester DWA1 under ABA while GID1s liberate it under GA.

ABA receptors (PYLs) directly bind RGL2 and block degradation of this master germination repressor.

Gibberellin receptors (GID1s) outcompete PYLs for RGL2 occupancy through superior binding affinity.

DWA1, a CUL4-DDB1 substrate receptor, functions as an executor of GA signaling by mediating RGL2 ubiquitination and degradation.

PYLs sequester DWA1 under ABA while GID1s liberate it under GA.

Stabilization of master germination repressor RGL2 integrates abscisic acid and gibberellin signalling during plant germination.