Daylength sensing in many plants is critical for coordinating the timing of flowering with the appropriate season. Temperate climate-adapted grasses such asBrachypodium distachyonflower during the spring when days are becoming longer. The photoreceptor PHYTOCHROME C is essential for long-day (LD) flowering inB.distachyon.PHYCis required for the LD activation of a suite of genes in the photoperiod pathway includingPHOTOPERIOD1(PPD1) that, in turn, result in the activation ofFLOWERING LOCUS T(FT1)/FLORIGEN, which causes flowering. Thus,B.distachyon phyCmutants are extremely delayed in flowering. Here we show that PHYC-mediated activation of PPD1 occurs viaEARLY FLOWERING 3(ELF3), a component of the evening complex in the circadian clock. The extreme delay of flowering of thephyCmutant disappears when combined with anelf3loss-of-function mutation. Moreover, the dampenedPPD1expression inphyCmutant plants is elevated inphyC/elf3mutant plants consistent with the rapid flowering of the double mutant. We show that loss ofPPD1function also results in reducedFT1expression and extremely delayed flowering consistent with results from wheat and barley. Additionally,elf3mutant plants have elevated expression levels ofPPD1, and we show that overexpression ofELF3results in delayed flowering associated with a reduction ofPPD1andFT1expression, indicating that ELF3 repressesPPD1transcription consistent with previous studies showing that ELF3 binds to thePPD1promoter. Indeed,PPD1is the main target of ELF3-mediated flowering aself3/ppd1double mutant plants are delayed flowering. Our results indicate thatELF3operates downstream fromPHYCand acts as a repressor ofPPD1in the photoperiod flowering pathway ofB.distachyon.