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Fig 1.

COP1 associates with CRY1 and CRY2 in a blue-light dependent manner in vivo.

(A, B) Co-immunoprecipitation of CRY1 (A) and CRY2 (B) by YFP-COP1. Transgenic 35S::YFP-COP1 seedlings were grown in darkness (D) for 4 days and subsequently transferred to blue light (B) of a fluence rate of 50 μmol m-2 s-1 for 1 h (A) or 5 min (B). Protein extracts were immunoprecipitated using α-GFP beads. YFP-COP1 was detected using α-GFP antibodies; CRY1 and CRY2 were detected using α-CRY1 and α-CRY2 antibodies. Asterisks likely indicate phosphorylated CRY1 and CRY2, respectively. All signals in (A) and (B) were from the same respective membrane. The YFP-COP1 signals (A, B) of the input samples were from longer exposures than those from the co-immunoprecipitates. The CRY1 signals (A) of the input samples were from shorter exposure than those from the co-immunoprecipitates.

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Fig 2.

The B-induced in vivo-association of COP1 with CRY1 requires SPA proteins, while COP1 associates with CRY2 independently of SPA.

(A, B) Co-immunoprecipitation of CRY1 (A) and CRY2 (B) by YFP-COP1 in a SPA wild-type (YFP-COP1) or spa null background (YFP-COP1 spaQn). Seedlings were grown in darkness for 4 days (D) and subsequently transferred to blue light (B) of a fluence rate of 50 μmol m-2 s-1 for 1 h (A) or 5 min (B). Protein extracts were immunoprecipitated using α-GFP beads. YFP-COP1 was detected using α-GFP antibodies. YFP-COP1 expression is very low and frequently only detectable after immunoprecipitation. CRY1 and CRY2 were detected using α-CRY1 and α-CRY2 antibodies. Asterisks likely indicate phosphorylated CRY1 and CRY2, respectively. The samples shown in (B) were on the same membrane with one lane digitally removed in the center.

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Fig 3.

Co-expression of SPA1 increases the interaction between COP1 and CRY1 in yeast three-hybrid experiments.

(A) Yeast two-hybrid assay analyzing the interaction between CRY1 and COP1. (B) Yeast three-hybrid assay analyzing the CRY1-COP1 interaction in the presence or absence of co-expressed SPA1. (C) Yeast three-hybrid assay analyzing the CRY1-SPA1 interaction in the presence or absence of co-expressed COP1. Co-transformed yeast cells were grown in darkness for 24 h and exposed to B (50 μmol m-2 s-1) or kept in darkness for 24 h before measuring ß-galactosidase activity. Error bars represent the SEM of three biological replicates. Asterisks indicate significant differences between the indicated comparisons (** p < 0.01, *** p < 0.001, n.s. not significant at p = 0.05).

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Fig 4.

A SPA1 deletion-protein defective in COP1-interaction shows no or a strongly reduced in vivo-association with CRY1 and CRY2, respectively.

(A) ΔCC SPA1-HA lacking the coiled-coil domain fails to interact with COP1 in vivo. Seedlings were grown in darkness for 4 d. (B, C) Co-immunoprecipitation of CRY1 (B) and CRY2 (C) by SPA1-HA and ΔCC SPA1-HA. Seedlings were grown in darkness for 4 days (D) and subsequently transferred to blue light (B) of a fluence rate of 50 μmol m-2 s-1 for 1 h (B) or 5 min (C). HA-tagged proteins were immunoprecipitated using α-HA-coupled beads. SPA1-HA and ΔCC SPA1-HA were detected using α-HA antibodies. CRY1 and CRY2 were detected using α-CRY1 and α-CRY2 antibodies. Asterisks likely indicate phosphorylated CRY1 and CRY2, respectively. Images in (B) separated by a vertical bar represent the same membrane which was exposed for different periods of time.

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