Plant-specific BLISTER interacts with kinase BIN2 and BRASSINAZOLE RESISTANT1 during skotomorphogenesis

Brassinosteroids play an essential role in promoting skotomorphogenesis, yet the underlying mechanisms remain unknown. Here we report that a plant-specific BLISTER (BLI) protein functions as a positive regulator of both BR signaling and skotomorphogenesis in Arabidopsis (Arabidopsis thaliana). We found that the glycogen synthase kinase 3 (GSK3)-like kinase BRASSINOSTEROID INSENSITIVE2 interacts with and phosphorylates BLI at 4 phosphorylation sites (Ser70, Ser146, Thr256, and Ser267) for degradation; in turn, BR inhibits degradation of BLI. Specifically, BLI cooperates with the BRASSINAZOLE RESISTANT1 (BZR1) transcription factor to facilitate the transcriptional activation of BR-responsive genes. Genetic analyses indicated that BLI is essentially required for BZR1-mediated hypocotyl elongation in the dark. Intriguingly, we reveal that BLI and BZR1 orchestrate the transcriptional expression of gibberellin (GA) biosynthetic genes to promote the production of bioactive GAs. Our results demonstrate that BLI acts as an essential regulator of Arabidopsis skotomorphogenesis by promoting BR signaling and GA biosynthesis. BLISTER facilitates Arabidopsis skotomorphogenesis by promoting brassinosteroid signaling and GA biosynthesis.

Automated summary

The plant-specific protein BLISTER acts as a positive regulator of BR signaling and skotomorphogenesis in Arabidopsis. It interacts with and phosphorylates BRASSINOSTEROID INSENSITIVE2 for degradation, while BR inhibits the degradation of BLISTER. BLISTER cooperates with the transcription factor BZR1 to activate BR-responsive genes and also regulates gibberellin biosynthesis for skotomorphogenesis in Arabidopsis.