Fig. 5. The dominant-negative form of Deltex (Dx^PRM) suppressed Notch signaling downstream of the full-length Notch and upstream of an activated form of Notch. (A) Notch and its derivative. Protein motifs in Notch: SP, a signal peptide; EGF, 36 EGF-like repeats; N, 3 Notch/Lin-12 repeats; TM, the transmembrane domain; NLS, two nuclear localization signals; ANK, 6 CDC10/Ankyrin repeats; opa, polyglutamine repeat. The full-length Notch and an activated form of Notch are shown at the top and bottom of A, respectively. N^act is a truncated form that lacks the entire extracellular domain and the transmembrane domain. It functions as a constitutively active form of Notch. (B-G) UAS-N^full or UAS-N^act was expressed alone or co-expressed with UAS-Dx^PRM under the control of the ptc-GAL4 driver. Wing discs of third-instar larvae are shown. (B) Overexpression of N^act. SOPs are shown in green. Note that a row of ectopic SOP cells was formed (arrowhead). (C) Co-expression of N^act and Dx^PRM (red). Ectopic formation of SOPs (green) was not suppressed. (D) Overexpression of N^act induced the ectopic expression of Wg (green) (Couso et al., 1994; Williams et al., 1994). (E) Co-expression of N^act and Dx^PRM (red). Note that the ectopic Wg expression (green) remained essentially the same. (F) Overexpression of N^full (red) induced the ectopic Wg expression (green). (G) Co-expression of N^full and Dx^PRM (red). Note that the ectopic expression of Wg (green) was suppressed.