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The maternal transcription factor VegT is important for establishing the primary germ layers in Xenopus. In previous work, we showed that the vegetal masses of embryos lacking maternal VegT do not produce mesoderm-inducing signals and that mesoderm formation in these embryos occurred ectopically, from the vegetal area rather than the equatorial zone of the blastula. Here we have increased the efficiency of the depletion of maternal VegT mRNA and have studied the effects on mesoderm formation. We find that maternal VegT is required for the formation of 90% of mesodermal tissue, as measured by the expression of mesodermal markers MyoD, cardiac actin, Xbra, Xwnt8 and alphaT4 globin. Furthermore, the transcription of FGFs and TGFbetas, Xnr1, Xnr2, Xnr4 and derrière does not occur in VegT-depleted embryos. We test whether these growth factors may be endogenous factors in mesoderm induction, by studying their ability to rescue the phenotype of VegT-depleted embryos, when their expression is restricted to the vegetal mass. We find that Xnr1, Xnr2, Xnr4 and derrière mRNA all rescue mesoderm formation, as well as the formation of blastopores and the wild-type body axis. Derrière rescues trunk and tail while nr1, nr2 and nr4 rescue head, trunk and tail. We conclude that mesoderm induction in Xenopus depends on a maternal transcription factor regulating these zygotic growth factors.
The mouse T (Brachyury) gene is required for early mesodermal patterning. Mice homozygous for mutations in T die at midgestation and display defects in mesodermal tissues such as the notochord, the allantois and the somitic mesoderm. To examine the role of T in patterning of somitic and posterior mesoderm along the anterior-posterior axis, we have examined the expression of a panel of molecular markers normally localized to the sub-set of cell types affected in TWis mutant mice. Through the use of whole-mount antibody double labelling techniques, we have analysed the spatial relationships of distinct mesodermal populations relative to cells expressing the T protein. We have also examined the consequences of the TWis mutation on mesodermal populations recognised by these markers. We demonstrate that TWis homozygous mutants retain the ability to form notochordal precursor cells, as identified both by the T antibody and the expression of sonic hedgehog/vertebrate homolog of hedgehog 1 (Shh/vhh-1) and goosecoid, however, these cells fail to proliferate or differentiate. These early notochordal defects appear to result in aberrant somitic differentiation as revealed by the distribution of mox-1 protein and twist RNA expression. Moreover, twist expression in paraxial mesoderm appears to be dependent on normal T activity, while Shh/vhh-1, goosecoid, mox-1 and cdx-4 are not T dependent. We propose that T is required for the maintenance of notochordal tissue and subsequent signals required for somite differentiation.