Skip to main content
. 2001 Apr;12(4):1177–1188. doi: 10.1091/mbc.12.4.1177

Figure 5.

Figure 5

Analysis of the effect of clustered point mutations in the minimal Arm-binding domain of DEC on its ability to bind Arm and β-catenin (βcat) in the yeast two-hybrid system. (A) Diagram of the DEC tail and sequences of the clustered point mutations used in this study, with the sequences of DE-cadherin (DE-Cad) and human E-cadherin (hE-Cad) in the region of the mutations shown below. All mutations were introduced into and analyzed in the context of the full-length cytoplasmic tail. The mutation DECM2 was also tested in the context of a smaller fragment of the cadherin tail (DEC30; Figure 1A)—this derivative is DEC30(M2). (B) The DE-cadherin mutants diagrammed in A were fused to the Gal4 transcription activation domain and transformed into yeast cells together with the full Arm repeat region of Arm or β-catenin (Arm R1–12 or βcat R1–12, left) or a smaller fragment of the Arm repeat region (Arm R2–10 or βcat R2–10, right), fused to the LexA DNA-binding domain. Average β-galactosidase activities are shown.