Figure 3.

Light-Mediated Proteolysis Controlled by ZTL, FKF1, and LKP2 in the Regulation of Flowering Time and the Circadian Clock.

(A) The function of FKF1 in the control of flowering time. GI forms protein complexes with CDFs on the CO promoter. In the afternoon, FKF1 is recruited to the CO promoter region through blue-light-dependent interaction with GI. FKF1 degrades CDFs, facilitating expression of CO. Since CDF2 is stabilized further in the ztl fkf1 lkp2 triple mutants than in the fkf1 mutants, the ZTL–GI and LKP2–GI complexes may also contribute to the degradation of some CDF proteins. CO and GI bind to the FT promoter and activate FT transcription, which induces flowering. FKF1 may also bind to the FT promoter; however, the function of this interaction is unknown.

(B) The function of ZTL in regulation of the circadian clock. Under blue light, ZTL interacts with GI. ZTL also forms a protein complex with HSP90. The interaction of ZTL with GI and HSP90 stabilizes ZTL protein. The ZTL–GI complex formation may sequester ZTL from interaction with TOC1 or PRR5. This enables TOC1 and PRR5 proteins to accumulate in the late afternoon. The FKF1–GI and LKP2–GI complex may also have a similar role (left side). In the dark, ZTL (FKF1 and LKP2) interact with TOC1 and PRR5 proteins and degrade them through a proteasome pathway (right side).