Trichome development is a fascinating model to elaborate the plant cell differentiation and growth processes. A wealth of information has pointed to the contributions of the components associated with cell cycle control and ubiquitin/26S proteasome system (UPS) to trichome morphogenesis, but how these two pathways are connected remains obscure. Here, we report that HECT-type ubiquitin ligase KAKTUS (KAK) targets the cyclin-dependent kinase (CDK) inhibitor KRP2 (for kip-related protein 2) for proteasome-dependent degradation during trichome branching in Arabidopsis. We show that over-expression of KRP2 promotes trichome branching and endoreduplication which is similar to kak loss of function mutants. KAK directly interacts with KRP2 and mediates KRP2 degradation. Mutation of KAK results in the accumulation of steady-state KRP2. Consistently, in kak pKRP2:KRP2-GFP plants, the trichome branching is further induced compared with the single mutant. Taken together, our studies bridge the cell cycle control and UPS pathways during trichome development and underscore the importance of post-translational control in epidermal differentiation.
Keywords: CDK inhibitor; KAKTUS; KRP2; endoreduplication; protein degradation; trichome branching.