Figure 9.
Schematic model illustrating the role of ELF3β. As a transcriptional repressor, the evening complex is recruited to the promoters of the target genes (including GI, PRR7, PIF4, and BBX6) via LUX. Full-length ELF3α serves as a scaffold to bring together ELF4 and LUX. ELF3β inhibits the function of ELF3α by forming a nonfunctional ELF3α–ELF3β heterodimer. Consequently, elevating ELF3β expression leads to early flowering, long hypocotyls, and an arrhythmic circadian clock, which is similar to the elf3-3 mutant phenotype. Without functional ELF3α, expressing ELF3β in the elf3-3 mutant does not significantly affect its early-flowering phenotype, suggesting that the function of ELF3β depends on ELF3α.

Schematic model illustrating the role of ELF3β. As a transcriptional repressor, the evening complex is recruited to the promoters of the target genes (including GI, PRR7, PIF4, and BBX6) via LUX. Full-length ELF3α serves as a scaffold to bring together ELF4 and LUX. ELF3β inhibits the function of ELF3α by forming a nonfunctional ELF3α–ELF3β heterodimer. Consequently, elevating ELF3β expression leads to early flowering, long hypocotyls, and an arrhythmic circadian clock, which is similar to the elf3-3 mutant phenotype. Without functional ELF3α, expressing ELF3β in the elf3-3 mutant does not significantly affect its early-flowering phenotype, suggesting that the function of ELF3β depends on ELF3α.

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