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Rice tillering, a key architecture trait determining grain yield, is highly regulated by a class of newly identified phytohormones, strigolactones (SLs). However, the whole SL signaling pathway from the receptor to downstream transcription factors to finally inhibit tillering remains unrevealed. In this study, we first found that brassinosteroids (BRs) strongly enhance tillering by promoting bud outgrowth in rice, which is largely different from the function of BRs in Arabidopsis. Genetic and biochemical analyses indicated that both the SL and BR signaling pathways control rice tillering by regulating the stability of D53 and/or the OsBZR1-RLA1-DLT module, a transcriptional complex in the rice BR signaling pathway. We further found that D53 interacts with OsBZR1 to inhibit the expression of FC1, a local inhibitor of tillering, and that this inhibition depends on direct DNA binding by OsBZR1, which recruits D53 to the FC1 promoter in rice buds. Taken together, these findings uncover a mechanism illustrating how SLs and BRs coordinately regulate rice tillering via the early responsive gene FC1., (Copyright © 2019 The Author. Published by Elsevier Inc. All rights reserved.)

Mesocotyl is the crucial organ for pushing buds out of deep water or soil after germination in monocots. Deep direct seeding or mechanized dry seeding cultivation practice requires rice cultivars having long mesocotyl. However, the mechanisms of mesocotyl elongation and domestication remain unknown. Here, our genome-wide association study (GWAS) reveals that natural variations of OsGSK2, a conserved GSK3-like kinase involved in brassinosteroid signaling, determine rice mesocotyl length variation. Variations in the coding region of OsGSK2 alter its kinase activity. It is selected for mesocotyl length variation during domestication. Molecular analyses show that brassinosteroid-promoted mesocotyl elongation functions by suppressing the phosphorylation of an U-type cyclin, CYC U2, by OsGSK2. Importantly, the F-box protein D3, a major positive component in strigolactone signaling, can degrade the OsGSK2-phosphorylated CYC U2 to inhibit mesocotyl elongation. Together, these results suggest that OsGSK2 is selected to regulate mesocotyl length by coordinating strigolactone and brassinosteroid signaling during domestication.

Brassinosteroids (BRs) are plant-specific steroid hormones that control plant growth and development. Recent studies have identified key components of the BR signaling pathway in Arabidopsis thaliana and in rice ( Oryza sativa ); however, the mechanism of BR signaling in rice, especially downstream of GSK3/SHAGGY-like kinase (GSK2), remains unclear. Here, we identified a BR-insensitive rice mutant, reduced leaf angle1 ( rla1 ), and cloned the corresponding gene. RLA1 was identical to the previously reported SMALL ORGAN SIZE1 ( SMOS1 ), which was cloned from another allele. RLA1/SMOS1 encodes a transcription factor with an APETALA2 DNA binding domain. Genetic analysis indicated that RLA1/SMOS1 functions as a positive regulator in the BR signaling pathway and is required for the function of BRASSINAZOLE-RESISTANT1 (OsBZR1). In addition, RLA1/SMOS1 can interact with OsBZR1 to enhance its transcriptional activity. GSK2 can interact with and phosphorylate RLA1/SMOS1 to reduce its stability. These results demonstrate that RLA1/SMOS1 acts as an integrator of the transcriptional complex directly downstream of GSK2 and plays an essential role in BR signaling and plant development in rice., (© 2017 American Society of Plant Biologists. All rights reserved.)

Leaf erectness is key in determining plant architecture and yield, particularly in cereal crops. Brassinosteroids (BRs) play a unique role in controlling this trait in monocots, but the underlying cellular and molecular mechanisms remain big mysteries. Here we report that the abaxial sclerenchyma cell number of rice lamina joints (LJs) is closely related to leaf erectness, and BR signaling tightly regulates their proliferation. We identified a rice U-type cyclin CYC U4;1 enriched in rice LJs, with its expression accompanying LJ development. Genetic and biochemical studies demonstrated that CYC U4;1 plays a positive role in promoting leaf erectness by controlling the abaxial sclerenchyma cell proliferation. Furthermore, BR signaling inhibits the abaxial sclerenchyma cell division by coordinately regulating CYC U4;1 expression through BES1 and CYC U4;1 protein activity through GSK3 kinases. These results support a key role of the cyclin CYC U4;1 in mediating BR-regulated cell division to control leaf erectness., (Copyright © 2015 Elsevier Inc. All rights reserved.)