Figure 1.

CKI1 expression under various light conditions (A to F) in wild-type, lph/hy1-7, and phyA seedlings. CKI1 expression was analyzed in 6-d-old ProCKI1:uidA seedlings grown under short day (short d; 8-h light/16-h darkness), darkness (D), continuous red (cR), and far-red (cFR) light (both 50 μmol m⁻² s⁻¹) and cR-low and cFR-low (both 2 μmol m⁻² s⁻¹). In the wild-type, developmental and light-controlled changes in CKI1 expression could be observed. Onset of etiolation leads to loss of CKI1 expression in the SAM, while it is up-regulated in the vasculature of hypocotyl and root transition zone. R light stimulates, but FR inhibits CKI1 activity. lph/hy1-7 disturbs light-dependent changes in CKI1 expression pattern and with some minor changes (see the main text), resembles the situation in the wild type under darkness. phyA largely phenocopies CKI1 expression in the lph/hy1-7. Note the absence of CKI1 activity in SAM of phyA under short-d and R conditions, suggesting phyA as a positive regulator of CKI1 in the absence of FR as the dominant light source. phyA mediates the negative effect of FR light on CKI1 activity indicated by persisting CKI1 expression in the phyA under FR conditions, suggesting the dual role of phyA in the control of CKI1. Arrows: Specific ProCKI1:uidA signal in individual tissues under the short d conditions. Red asterisk: Conditions leading to etiolation-specific CKI1 expression pattern. Black arrowhead: ProCKI1:uidA signal specific for etiolated seedling phenotype, shown only on wild type as an example. White arrowhead: CKI1 specific signal related to partially etiolation response under low light intensity. Scale bars: 100 μm. CL, cauline leaf; SAM, shoot apical meristem; H, hypocotyl; RSJ, root, shoot junction; RT, root tip.