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Fig. 3 Co-injection of RNA encoding heterodimeric xRXRβ and xRARα2 results in the formation of ectopic neurons at the tailbud stage. Dorsal views of embryos stained by wholemount in situ hybridisation for XIF3 at the tailbud stage, (anterior to the right). Embryos were injected with: (A) xRARα2/xRXRβ, (B) xRARα2, (C) xRXRβ, (D) xRARα2∆h*d, (E) xRARα2∆h*d/RXRβ; (F) was uninjected. Co-injection of xRARα2/xRXRβ results in embryos that have abnormal patterns of XIF3 expression with positive regions adjacent to the neural tube (e.g. arrow in A). However injection of individual receptors (B,C) or a combination of control transcript xRARα2∆h*d and xRXRβ (E) has no effect on XIF3 expression. Embryos injected in an identical manner were assayed with the anti- HNK1 monoclonal antibody to demonstrate the formation of ectopic neurons. (G) xRARα2/xRXRβ-injected and (H) uninjected embryos rendered transparent in Murray�s clear to see neural cell bodies. Axons (arrows) are apparent in both embryos but ectopic clusters of anti-HNK1 positive cell bodies (arrowheads) are only seen adjacent to the neural tube in xRARα2/xRXRβ injected embryos (G) and not in controls (H). |
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Fig. 5. Ectopic neurons form even when cell proliferation is inhibited in neural precursors. Embryos at the early gastrula stage were treated with hydroxyurea and aphidicolin (HUA) to inhibit cell division (Harris and Hartenstein, 1991) and assayed for XIF3 at the tailbud stage. XIF3 staining is somewhat punctate along the neural tube of uninjected and control xRARα2∆h*d/xRXRβ- coinjected embryos, probably reflecting the HUA treatment. Coinjection of xRARα2/xRXRβ, however, generates ectopic neurons both in untreated and HUA-treated embryos (arrowheads). It is therefore likely that the ectopic neurons do not form through increased proliferation of neural precursors. |
