Fig. 7. March2 antagonizes canonical Wnt signaling in concert with Dapper1 for head formation. (A) Dpr1MO impairs the March2-mediated decrease of activated β-catenin and phosphorylated LRP6 levels. Amounts of injected mRNAs and MOs: Wnt8, 20 pg; March2, 1 ng; CoMO, 40 ng; Dpr1MO, 20 and 40 ng, respectively; Dpr1, 1 ng. (B) DN Dpr1 mRNA (2 ng) impedes the March2 mRNA (1 ng)-mediated decrease of activated β-catenin. (C) Rescuing ability of March2 mRNA (1 ng) for the Wnt8 DNA (40 pg)-mediated head defect was impeded by Dpr1MO (40 ng). ‘Severe’ denotes eyeless, malformation of cement glands and loss of anterior head structures. ‘Mild’ denotes small sizes of eyes and head. Statistical analysis was carried out on three independent experiments. P values were obtained using two-tailed Student’s t-test (see also Table S3). (D) Malfunction of endogenous March2 by moderate doses of Mar2MO (20 ng) and Dpr1MO (20 ng) induced head defects (see also Table S3). (E) Model for March2-mediated Dsh degradation in Xenopus. Upon Wnt stimulation, Dsh relays signal for downstream gene transcription. To maintain the Wnt-off state, reduction of the cytosolic pool of Dsh is required. For this purpose, March2 binds and ubiquitylates Dsh in concert with Dpr1 for lysosomal degradation.
Image published in: Lee H et al. (2018)
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