Abstract
SLR1 acts as a repressor of gibberellin (GA) signaling. GA perception by GA receptor GID1 causes SLR1 degradation involving the F-box protein GID2. In GA-insensitive and GA-deficient mutants, SLR1 accumulates and the severity of dwarfism is usually correlated with the level of SLR1 accumulation. An exception is the GA-insensitive F box mutant gid2, which shows milder dwarfism than mutants such as gid1 and cps even though it accumulates higher levels of SLR1. Here, we investigate on such mutant phenotype in gid2.
In gid2, loss of GID1 function or treatment with a GA biosynthesis inhibitor decreased the level of SLR1 and enhanced its dwarfism. On the contrary, overproduction of GID1 or treatment with GA3 increased the SLR1 level in gid2 and reduced its dwarfism. These results indicate that de-repression of SLR1 repressive activity can be accomplished only by GA and GID1 but not require the F-box (GID2) function.
