Plants possess a large family of receptor kinase proteins to mediate cell-to-cell and cell-to-environment communication, and these regulations are essential for plant growth and development as well as resistance to biotic or abiotic stresses. EMS1 is a receptor kinase which involved in tapetum cell fate determination during anther development, while brassinosteroid (BR) receptor, BRI1, controls most aspects of plant growth and development. Although EMS1 and BRI1 are known to regulate independent biological processes, they interact with identical components of the downstream signaling pathways. However, the biological processes other than the tapetum development controlled by the EMS1 signal are not clear. Here, we report that EMS1 signaling-related mutants exhibited an insufficient stamen elongation phenotype, similar to BR signaling mutants. Transgenic expression of BRI1 restored the short filament phenotype of ems1. Conversely, co-expression of EMS1 and TPD1 also restored the short filaments of BRI1 mutants, bri1. Genetic experiments confirmed that EMS1 and BRI1 regulate filament elongation through their downstream transcription factors BES1/BZR1. Molecular analysis suggested that the decrease in BR signaling output in filaments of the ems1 mutant caused deficient filament development. Moreover, in vitro and in vivo experiments proved BES1 interacts with filament-specific transcription factor MYB21. Together, we found that the two receptor-like kinases (RLKs) EMS1 and BRI1 are cooperatively involved in the regulation of filament elongation via the transcription factors BES1/BZR1. These results indicated that the biological processes regulated by EMS1 and BRI1 in plants are both independent and interactive, which provides us with insights into multidimensional molecular control of the RLK pathway.
Keywords: BES1/BZR1; Brassinosteroids; EMS1; Stamen elongation.
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