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The T Gene Is Necessary for Normal Mesodermal Morphogenetic Cell Movements During Gastrulation

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The T Gene Is Necessary for Normal Mesodermal Morphogenetic Cell Movements During Gastrulation Development 121, 877-886 (1995) 877 Printed in Great Britain © The Company of Biologists Limited 1995 The T gene is necessary for normal mesodermal morphogenetic cell movements during gastrulation Valerie Wilson1, Linda Manson2, William C. Skarnes3 and Rosa S. P. Beddington1 1Laboratory of Mammalian Development, National Institute for Medical Research, London NW7 1AA, UK 2Biomedical Research Centre, University of Dundee, Ninewells Hospital, Dundee DD1 9SY, UK 3Centre for Genome Research, Edinburgh EH9 3JQ, UK SUMMARY The T (Brachyury) deletion in mouse is responsible for parison of T expression in the developing tailbud with the defective primitive streak and notochord morphogenesis, sites of accumulation of T/T cells in chimeras shows that leading to a failure of the axis to elongate properly T/T cells collect in sites where T would normally be posterior to the forelimb bud. T/T embryonic stem (ES) expressed. T expression becomes internalised in the tailbud cells colonise wild-type embryos, but in chimeras at 10.5 following posterior neuropore closure while, in abnormal days post coitum (dpc) onwards they are found predomi- chimeric tails, T/T cells remain on the surface of the distal nantly in the distal tail, while trunk paraxial and lateral tail. We conclude that prevention of posterior neuropore mesoderm are deficient in T/T cells (Wilson, V., Rashbass, closure by the wedge of T/T cells remaining in the primitive P. and Beddington, R. S. P. (1992) Development 117, 1321- streak after gastrulation is one source of the abnormal tail 1331). To determine the origin of this abnormal tissue dis- phenotypes observed. tribution, we have isolated T/T and control T/+ ES cell Accumulation of T/T cells in the node and anterior streak clones which express lacZ constitutively using a gene trap during gastrulation results in the preferential incorpora- strategy. Visualisation of T/T cell distribution in chimeric tion of T/T cells into the ventral portion of the neural tube embryos throughout gastrulation up to 10.5 dpc shows that and axial mesoderm. The latter forms compact blocks a progressive buildup of T/T cells in the primitive streak which are often fused with the ventral neural tube, remi- during gastrulation leads to their incorporation into the niscent of the notochordal defects seen in intact mutants. tailbud. These observations make it likely that one role of Such fusions may be attributed to cell-autonomous changes the T gene product is to act during gastrulation to alter cell in cell adhesion, possibly related to those observed at surface (probably adhesion) properties as cells pass earlier stages in the primitive streak. through the primitive streak. As the chimeric tail elongates at 10.5 dpc, abnormal mor- Key words: T (Brachyury), ES cell, chimera, mouse embryo, phology in the most distal portion becomes apparent. Com- gastrulation INTRODUCTION during the early stages of gastrulation, since development rostral to the forelimb bud appears grossly normal. Only in more caudal The T gene is deleted in mouse Brachyury mutants (Herrmann trunk regions and in later embryos is the notochord missing and et al., 1990) causing a reduction in tail length in hemizygotes other mesodermal derivatives deficient or defective (Herrmann, and death of homozygous embryos on the 11th day of gestation 1992; Beddington et al., 1992; Rashbass et al., 1994). One expla- (Chesley, 1935; Gluecksohn-Schonheimer, 1944; Gruneberg, nation for this would be that T is only required once all tissues 1958). The T gene encodes a putative transcription factor rostral to the forelimb have been laid down (i.e. after the 1- to (Kispert and Herrmann, 1993) and both its mRNA and protein 2-somite stage). The demonstration that wild-type T protein is are present in the primitive streak from the onset of gastrulation only required from the 9th day of gestation for continuation of (Wilkinson et al., 1990; Herrmann, 1991; Kispert and Herrmann, its own expression (Herrmann, 1991) and that of certain other 1994). Expression persists in the streak and later in the tailbud genes (Wnt-3a, Wnt-5a (McMahon, 1992), Evx-1 (Dush and for the entire period of axis formation and axis elongation (6.5- Martin, 1992)) transcribed in the streak (Rashbass et al., 1994) 12.5 dpc; Kispert and Herrmann, 1994). It is also expressed in is consistent with such an hypothesis. However, the chimeric the node and notochord. The pattern of T expression appears to studies reported in this paper indicate that T is necessary for be essentially identical in vertebrates where its homologue has normal morphogenetic movements during earlier stages of gas- been studied (Smith et al., 1991; Schulte-Merker et al., 1992). trulation. However, the phenotype of homozygous mutant mouse embryos We have shown previously that abnormalities characteristic does not obviously correlate with an essential function for T of T/T embryos occur in chimeras made between T/T mutant 878 V. Wilson and others cells and wild-type ones (Rashbass et al., 1991). Using a 6% CO2 in air. Subsequently the dishes were inverted, the drops glucose phosphate isomerase isozyme variant as a genetic covered with paraffin oil (Boots, UK, Ltd) and incubated overnight. marker to distinguish mutant cells, we found that T/T cells in Embryos that had developed to the blastocyst stage were transferred 9.5-11.5 dpc chimeras were unevenly distributed along the to pseudopregnant recipients. embryonic craniocaudal axis (Wilson et al., 1993; Beddington Recovery and staining of chimeras et al., 1992). Mutant cells predominated in caudal regions and Potential chimeras were dissected from the uterus 5-8 days following were relatively sparse in mesodermal derivatives compared to transfer. Fixation and X-gal staining of embryos was as described else- non-ingressing ectodermal tissues. This led to the hypothesis where (Beddington et al., 1989). Embryos up to 8.5 dpc were fixed for that mutant cells ingressing through the streak were defective 10-20 minutes, whereas later stages were fixed for 20-30 minutes. The compared to wild-type cells (with which they were in compe- duration of staining varied according to the ES cell clone used and tition) in their ability to move away from the midline and to ranged from 1 hour to 24 hours. Embryos showing positive staining populate the mesoderm at a normal rate. As a result, mutant were processed for wax histology as described in Beddington (1994), cells accumulate in the region responsible for axial elongation, and 7 µm serial sections were cut (Bright 6030 Microtome). Once and eventually inhibit it. By virtue of a transgenic single cell dewaxed, sections were mounted in DPX mountant (BDH, Ltd.) and marker introduced into mutant cells, we can now verify that photographed (Kodak Ektachrome 64T film) in a Zeiss Axiophot T/T cells start to amass in the primitive streak during gastrula- microscope using differential interference contrast optics. tion. These results demonstrate that wild-type T protein does Whole-mount in situ hybridisation have a function during the earlier stages of gastrulation. They The T mRNA probe was synthesised as described (Wilson et al., 1993) suggest that at least one of its early roles is to regulate the mor- and in situ hybridisation was performed according to Wilkinson phogenetic behaviour of nascent mesoderm by altering cell (1992). autonomous properties, probably related to cell adhesion. RESULTS MATERIALS AND METHODS Isolation and validation of ubiquitously expressing Vectors lacZ ES cell clones The gene trap vectors pGT1,2 and 3 contain the βgeo reporter Following electroporation and drug selection, 210 T/T ES cell (Friedrich and Soriano, 1991), flanked by the En-2 splice acceptor and β SV40 polyadenylation signal from pGT4.5 (Gossler et al., 1989). The clones and 229 T/+ clones were tested for bacterial -galac- En-2 exon sequence was modified to generate three derivatives which tosidase activity in 96-well plates. Approximately half of the can form fusion proteins in one of each of the three reading frames. clones of each genotype were positive (β-gal+) and of these, 21 Equal quantities of each vector were mixed together for electropora- (17.8%) T/T clones and 22 (17.7%) T/+ clones showed blue tion. staining in all cells in the well (Table 1). Four T/T and 5 T/+ strongly staining clones were selected for testing in chimeras Isolation of gene trap ES cell lines ubiquitously expressing lacZ (Table 2). Like the parent cell line (Wilson et al., 1993), the four T/T clones gave rise to chimeras showing a range of abnor- ES cells were maintained as described previously (Wilson et al., 1993). 108 ES cells (either ES line BTBR6 (T/T) or BTBR7 (T/+)) malities (Table 3) depending on the extent of mutant cell con- were electroporated with a mixture of gene trap vectors pGT1,2 and tribution (Fig. 1A,B). A high contribution of T/T cells (greater 3 using standard conditions (Hill and Wurst, 1993) and selected in than about 60%) produced detectable abnormalities by early medium containing G418 (200 µg/ml, Gibco). After 10 days of somite stages reminiscent of the intact T/T phenotype. Chimeras selection, 200-250 macroscopic colonies from each electroporation with a low T/T cell contribution exhibited tail and allantoic were picked into 96-well plates (Nunc) and grown for 3 days in the deformities, most evident from approximately 10.0 dpc. absence of drug selection. Each clone was then passaged into Although carrying independent gene trap insertions, all four T/T duplicate wells in separate 96-well plates and grown overnight. One clones behaved similarly in chimeras (Table 3), indicating that plate was stained with X-gal (Sigma) as described (Beddington et al., the hemizygous transgene was developmentally neutral.
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