Figure 9.

Model for Control of Seed Germination by SLY1 and RGL2.

(A) There is an alternative pathway controlling seed germination that is stimulated by GA. This pathway may bypass the sly1 mutation either by inhibiting RGL2 activity without causing decreased RGL2 protein levels possibly by posttranslational modification or by activating seed germination independently of SLY1/RGL2.

(B) In the ga1-3 mutant (no GA), RGL2 does not interact with the GA receptor GID1. In this case, RGL2 functions purely as a negative regulator. Addition of GA rescues ga1-3 seed germination by causing RGL2 to be destroyed following interaction with GA-GID1 and SCF^SLY1. In the sly1 mutant (GA present), RGL2 cannot be destroyed because SLY1 is defective. In this case, RGL2 acts as a repressor of GA responses when not bound to GID1, and GA-GID1-RGL2 may be inactive as a repressor or act as a positive regulator of seed germination.