Abstract
Leaf architecture directly determines canopy structure, and thus, grain yield in crops. Leaf droopiness is an agronomic trait primarily affecting the cereal leaf architecture but the genetic basis and underlying molecular mechanism of this trait remain unclear. Here, we report that DROOPY LEAF1 (DPY1), an LRR receptor-like kinase, plays a crucial role in determining leaf droopiness by controlling the brassinosteroid (BR) signaling output inSetaria, an emerging model for Panicoideae grasses. Loss-of-function mutation in DPY1 led to malformation of vascular sclerenchyma and low lignin content in leaves, and thus, an extremely droopy leaf phenotype, consistent with its preferential expression in leaf vascular tissues. DPY1 interacts with and competes for SiBAK1 and as a result, causes a sequential reduction in SiBRI1–SiBAK1 interaction, SiBRI1 phosphorylation, and downstream BR signaling. Conversely, DPY1 accumulation and affinity of the DPY1–SiBAK1 interaction are enhanced under BR treatment, thus preventing SiBRI1 from overactivation. As such, those findings reveal a negative feedback mechanism that represses leaf droopiness by preventing an overresponse of early BR signaling to excess BRs. Notably, plants overexpressing DPY1 have more upright leaves, thicker stems, and bigger panicles, suggesting potential utilization for yield improvement. The maize ortholog of DPY1 rescues the droopy leaves indpy1, suggesting its conserved function in Panicoideae. Together, our study provides insights into how BR signaling is scrutinized byDPY1to ensure the upward leaf architecture.
Funder
National Key Research and Development Program of China
National Natural Science Foundation of China
Key Research Program of Chinese Academy of Science
China Agricultural Research System
Science and Technology Innovation Project of Chinese Academy of Agricultural Science
Fundamental Research Funds of Chinese Academy of Agricultural Science
Natural Science Foundation of Hebei Province
Science and Technology Service Network Initiative of Chinese Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Cited by
45 articles.
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