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FIG. 4. Perturbations in Notch signaling cause defects in pronephric duct morphology. GR-Su(H)VP16- (activated) or GRSu( H)DBM- (dominant negative) injected embryos were examined by either whole-mount in situ hybridization or antibody staining using the following markers of duct formation: Lim-1, c-ret, and 4A6 epitope. As a control, injected sibling embryos were reared in the absence of dexamethasone, which resulted in minimal effects on duct marker expression (no dexamethasone GR-Su(H)DBMinjected embryos Lim-1 16% n 5 103, 4A6 10%n 5 69, c-ret 16% n 5 63; no dexamethasone GR-Su(H)VP16-injected embryos Lim-1 15% n 5 459, 4A6 18% n 5 83, c-ret 15% n 5 82). Injected, dexamethasone-treated embryos resulted in dramatic effects on duct marker expression on the injected side of the embryo compared to the uninjected side (dexamethasone-treated GR-Su(H)DBM embryos Lim-1 69% n 5 174, 4A6 72% n 5 148, c-ret 53% n 5 103; dexamethasone-treated GR-Su(H)VP16 embryos Lim-1 77% n 5 408, 4A6 88% n 5 213, c-ret 73% n 5 261). Fewer than 10% of uninjected dexamethasone-treated embryos showed asymmetry of all markers examined comparing the left and right sides of the embryo (data not shown). A change (either an increase or decrease) of molecular markers of the pronephros was determined by visual inspection of the injected side of the embryo compared to the uninjected control side of the embryo by two independent investigators.

Image published in: McLaughlin KA et al. (2000)

Copyright © 2000. Image reproduced with permission of the Publisher, Elsevier B. V.

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