XB-IMG-44082
Xenbase Image ID: 44082
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Fig. 7. In order to convert the V2.1.1 lineage to a retinal fate endo-mesodermal factors must be blocked in combination with suppression of BMP and Wnt signaling. (A) Expression domains of mesodermal (Xbra) and endodermal (sox17α, edd) genes are reduced by VegTMO injection into the vegetal pole, whereas controls (β-gal, cMO, cVegTMO) have no effects. (B) The extent to which the hindgut (g) is populated by V2.1.1 progeny (green) is strikingly reduced in VegTMO embryos (*) compared to controls (GFP). a, archenteron; s, somite. (C) Ectopic expression of rx1 (blue, arrows) in the vegetal pole was monitored by in situ hybridization after the V2.1.1 blastomere was injected with the indicated constructs. Red cells indicate the V2.1.1 progeny expressing those constructs. Reduction of VegT alone (VegTMO) or in combination with Vg1 (VegTMO/dnVg1) was not sufficient to induce ectopic rx1 expression. The long form of Cerberus (Cer-L), which can inhibit BMP, Wnt and Nodal signaling, was effective whereas the short version of Cerberus (Cer-S), which can inhibit only Nodal signaling, was not. Although reduction of both BMP signaling (by expression of noggin [Nog] and a dominant-negative BMP receptor [tBR]) and Wnt signaling (by expression of a dominant-negative Wnt8 construct [dnWnt]) causes ectopic rx1 expression, the cells expressing rx1 are not derived from the V2.1.1 clone (red cells), demonstrating an indirect consequence of the induction of a secondary head (as reported in Moore and Moody, 1999). However, combining the reduction of VegT or VegT plus Vg1 with the inhibition of BMP and Wnt signaling caused the V2.1.1 clone to ectopically express rx1, equivalent to the Cer-L phenotype. Image published in: Yan B and Moody SA (2007) Copyright © 2007. Image reproduced with permission of the Publisher, Elsevier B. V.
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