Here, we unveil a receptor-competition paradigm where ABA receptors (PYLs) stabilize RGL2 ... GA receptors (GID1s) counteract this stabilization by competitively displacing PYLs from RGL2.
First-pass extracted concept
direct receptor competition
Candidate: concept label1 source documents5 linked claims
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Aliases
direct receptor competition, receptor-competition paradigm
Evidence Snippets
Supporting Sources
Linked Claims
Direct receptor competition is presented as a complementary layer to hormone crosstalk and as a general framework for signal-driven developmental transitions.
Quoted textsource-backed
Our work establishes direct receptor competition as a complementary layer to hormone crosstalk, providing a universal framework for signal-driven developmental transitions.
Genetic epistasis supports that PYLs act upstream of DWA1 and compete directly with GID1 at RGL2.
Quoted textsource-backed
Genetic epistasis confirms that PYLs act upstream of DWA1, competing directly with GID1 at RGL2.
ABA receptors PYLs stabilize RGL2 through direct physical interaction and through functional sequestration of DWA1.
Quoted textsource-backed
ABA receptors (PYLs) stabilize RGL2, both through direct physical interaction and through functional sequestration of DWA1
GA receptors GID1s competitively displace PYLs from RGL2 and thereby license DWA1-mediated RGL2 degradation.
Quoted textsource-backed
GA receptors (GID1s) counteract this stabilization by competitively displacing PYLs from RGL2, leveraging their superior binding capacity to license DWA1-mediated degradation.
The balance of ABA and GA concentrations regulates PYL and GID1 expression and thereby defines receptor competition at RGL2.
Quoted textsource-backed
Crucially, this competition is defined by the concentration of abscisic acid and gibberellin as they regulate PYL and GID1 expression.