Abstract

In temperate and boreal perennial trees, precise timing of growth cessation under short photoperiods is essential for survival and geographic adaptation. In Populus, the circadian evening complex (EC) component EARLY FLOWERING 3 (ELF3) integrates temperature and photoperiod signals to regulate growth cessation, yet the underlying mechanism remains incompletely understood. Here, we demonstrate that the tree LUX ARRHYTHMO (LUX) homologs LUX1 and LUX2 interact with ELF3.1 to form functional EC. Mutant analyses show that elf3.1 single and lux1/2 double mutants fail to cease growth under short days, correlating with sustained FT2 expression. Mechanistically, the EC directly binds the promoters of FT2, GI/GIL, and FKF1a/b and represses their expression. Conversely, the GI-FKF1 complex physically interacts with EC components to counteract their repression on FT2. These findings reveal a reciprocal transcriptional-translational feedback circuit between the EC and GI-FKF1 modules that fine-tunes FT2 expression, ensuring precise photoperiodic control of seasonal growth in trees.