The circadian clock protein CmLHY integrates strigolactone signaling to regulate short-day-induced flowering in chrysanthemum.

Abstract

Flowering is a key ornamental trait in chrysanthemum and a major agronomic trait affecting rice yield. Strigolactones (SLs) are a class of phytohormones that regulate diverse aspects of plant growth and development, including flowering time. However, the molecular mechanisms underlying SL-mediated regulation of flowering remain poorly understood. Here, we show that SL promotes flowering in chrysanthemum under inductive short-day conditions. The SL-specific signaling complex CmMAX2-CmD14.1-CmD53 was first identified in chrysanthemum. Silencing CmD14.1 or CmMAX2 causes late-flowering and SL insensitivity, while their overexpression accelerates flowering upon SL treatment. In contrast, overexpression of CmD53 or the degradation-resistant variant CmD53m delayed flowering. SL-induced CmD53 degradation depends on both CmD14.1 and CmMAX2. RNA-seq analysis reveals that overexpression of CmD53 or CmD53m significantly downregulates the florigen gene CmFTL3. We confirmed that CmD53 directly binds to the CmFTL3 promoter to repress its transcription, thereby delaying flowering. Moreover, the central circadian clock protein CmLHY represses CmMAX2 and CmD14.1 transcription and subsequently modulates SL-mediated CmD53 degradation. This regulatory cascade fine-tunes CmFTL3 expression and controls flowering in chrysanthemum under inductive SD conditions. Similarly, in rice, OsD3 (a MAX2 homolog) and OsD14 act downstream of OsCCA1 (an LHY/CCA1 homolog) to regulate flowering. Our findings demonstrate that LHY/CCA1-mediated integration of SL signaling in the flowering regulatory pathway is conserved between chrysanthemum and rice, providing new insights into the novel crosstalk between the circadian clock and SL signaling in flowering-time control.