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. 2002 Sep 15;16(18):2403–2414. doi: 10.1101/gad.1011402

Figure 6.

Figure 6

SCFSlimb complex and a Cul3-based degradation machinery to control the CiFL stability in the anterior and posterior cells of the eye discs, respectively. (AD) The Cul1-based, SCFSlimb complex functions in the anterior cells to promote CiFL proteolytic processing. In the Cul1EX (A) and slimb1 (C) mutant clones located anterior to the MF, CiFL accumulation is detected (red), whereas in the posterior clones, no accumulation can be observed. The mutant clones of Cul1EX (B) and slimb1 (D) are marked by the lack of GFP expression. (E,F) In the Cul3gft2 mutant clones, marked by the lack of GFP expression (green), only posterior clones accumulate CiFL (red). (G,H) The ubiquitous expression patterns of Cul1 (G) and Cul3 (H) in the eye discs as revealed by in situ hybridization with antisense probes of Cul1 and Cul3, respectively. In the control experiments, the sense probes gave no signals (data not shown). (I) The phylogenetic tree of the Drosophila Cullin family (denoted by Dm) to their human counterparts (Hs).