Xenbase Image ID: 74579

Figure S9. Misexpression of XdnTcf7l2 in Xenopus laevis embryos results in multiple developmental anomalies. (A) As in the mouse, Tcf7l2 and dnTcf7l2 in Xenopus exist in multiple isoforms due to alternative splicing of exons 13-16. We identified the indicated XdnTcf7l2 isoforms, designated 1-4, as most abundant in stage 13 and 24 embryos, with their relative abundance at each stage indicated as a percentage. Color coding of XdnTcf7l2 protein domains within exons is as for Figure 3. X indicates the presence of a stop codon. Isoforms 1-3 contain the short SFLSS motif of Pukrop et al. (2001) in exon 9 (indicated by , while isoform 4 does not (indicated by . (B) We injected mRNAs encoding the indicated isoforms, either singly or in combination (1+2 and 3+4), into either the two dorsal blastomeres (orsal injections or one ventral blastomere (entral injections of 4-cell-stage embryos, with nuclear -galactosidase mRNA co-injected as a marker (or control). Embryos were scored for the indicated patterning phenotypes at st. 30-32. N indicates number of embryos scored. (C) Selected examples of patterning defects observed. Although these studies indicate that XdnTcf7l2 has potent developmental effects in vivo, there are two important caveats to interpreting these effects in a biological context. First, we are over-expressing exogenous XdnTcf7l2 much earlier in development than its normal first appearance at st. 13, and therefore may be affecting developmental events in which XdnTcf7l2 does not participate. And second, it is possible that this early expression of XdnTcf7l2 interferes with (inhibits) the activity of other XTcf proteins that may act earlier in development than does XTcf7l2. Image published in: Vacik T et al. (2011) Copyright © 2011. Image reproduced on with permission of the Publisher, Cold Spring Harbor Laboratory Press. This is an Open Access article. Larger Image Printer Friendly View

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