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Many molecules induce the ectopic expression of tissue-specific genes in Xenopus embryos. Conversely, interfering with their activity disrupts patterns of gene expression, implicating them in normal development. Does this mean that they control cell fate (i.e. position, as well as differentiation)? Xsox17alpha and beta can induce ectopic expression of endodermal markers; inhibiting their function suppresses expression of endodermal marker genes in the developing gut (Cell 91 (1997) 397). Here we show the effect of these manipulations on cell lineage. Expressing Xsox17 in a cells normally fated to become ectoderm causes their descendants either to relocate into the embryonic gut or to die at a late developmental stage. Conversely, disrupting Xsox17 activity in cells normally fated to be endodermal causes them to enter mesodermal and ectodermal lineages.
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11091074
???displayArticle.link???Mech Dev
Fig. 1. Fate map adapted from Dale and Slack (1987) showing the contribution of blastomeres at the 32-cell stage to a range of tissues.
Fig. 2. (A,B) Effects of injection of Xsox17β or Xsox17β::EnR RNA, with β-galactosidase RNA, into a single blastomere (as indicated) at the 32-cell stage of embryogenesis. Tadpoles were fixed and stained for β-galactosidase expression at stage 42. At least 50 embryos were analysed for each injection; those shown are typical of the results obtained. (C) Embryos from a single experiment (n=20) were scored at stage 42 for the presence of β-galactosidase-positive cells in a range of tissues. For each embryo the proportion of such cells in each tissue was scored from igh(++++) to ow(+). These data were then converted into the histograms above (although only representative examples of tissues are shown). Although a somewhat subjective approach, data from large numbers of embryos can be represented in this way, and the results from control embryos agree well with published fate maps.
Fig. 3. Histological analysis of embryos reveals the distribution of the labelled cells in embryos from the experiments depicted in Fig. 2. (A) Descendants of a control A-tier cell injected only with β-galactosidase mRNA are found in the epidermis (Ep) and are absent from the underlying gut. (B) If the cell is additionally injected with Xsox17β, there is no contribution to the epidermis, and clones of cells (arrowed) are found integrated into the gut endoderm. (C) These clones can be seen to be part of a histologically normal structure, as is shown by a section through the hindgut region where lineage labelled cells are indistinguishable from their unlabelled neighbours. (D) D-tier cell descendants are predominantly found in the gut endoderm with a smaller contribution to mesodermal derivatives such as somite (S). (E) Co-injection of Xsox17β::EnR results in a much reduced endodermal contribution, with more extensive localisation in lateral mesoderm (Mes), including somites (S) mesenchyme, and paired cardinal veins. Scale bar, 100 μm.
Fig. 4. The behaviour of lineage labelled cells during embryogenesis. (A) At stage 19 (late neurula) A-tier-derived clones are dispersed in the epidermis. (B) A-tier descendants expressing Xsox17β, however, tend to aggregate at this stage, producing dense swirling patterns. Superficial cells are still evident in these embryos at tailbud stages (D), although the number of labelled cells is reduced relative to the controls (C). Control D-tier clones (E), and those expressing Xsox17β::EnR (G), are internal during gastrula stages, and can only be visualised in cleared embryos (stage 10.5, (F) controls, (H) Xsox17β::EnR). By stage 19, control clones remain internal (I), while cells expressing Xsox17β::EnR are appearing on the surface of the embryo (J).
