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Conversion of a mesodermalizing molecule, the Xenopus Brachyury gene, into a neuralizing factor.

Y Rao
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Abstract

It has been shown previously that a Xenopus homolog of the mouse gene Brachyury, Xbra, can initiate mesodermal differentiation. Here, I report that a Xbra mutant truncated at the carboxyl terminus, B304, has lost the mesodermalizing activity and can block the activity of the wild-type Xbra. Injection of B304 mRNA led to formation of neural structures in animal cap explants. Examination of molecular markers in B304-injected explants shows expression of anterior neural markers in the absence of mesodermal markers, indicating that B304 can cause neuralization without the mediation of mesoderm. Implications of these findings on intracellular mechanisms underlying the initiation of neural differentiation in the ectodermal cells are discussed.

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ActivinsAnimalsBase SequenceBiomarkersCell Adhesion Molecules, NeuronalCell DifferentiationDNA-Binding ProteinsFetal ProteinsFibroblast Growth Factor 2FollistatinForkhead Transcription FactorsGlycoproteinsInhibinsMesodermMolecular Sequence DataMutationNervous SystemNuclear ProteinsSequence DeletionStructure-Activity RelationshipT-Box Domain ProteinsTranscription FactorsXenopusBrachyury ProteinJournal ArticleResearch Support, Non-U.S. Gov't

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Y Rao. 1994-04-15. Conversion of a mesodermalizing molecule, the Xenopus Brachyury gene, into a neuralizing factor.. https://doi.org/10.1101/gad.8.8.939

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