The tissue-specific transcription factor HNF1alpha is expressed in kidney, liver, intestine and stomach of Xenopus. We show that the HNF1alpha gene is transcriptionally activated at the onset of zygotic gene transcription and that this transcription is maintained throughout development. Ectodermal explants of blastulae (animal caps) express HNF1alpha mRNA upon stimulation with the mesoderm inducers activin A and BMP4 as well as on overexpression of Smad2 and Smad1, the corresponding members of the intracellular TGF-beta signal transducers, respectively. Beside these factors that mediate their response through serine/threonine kinase receptors, bFGF, which acts via tyrosine kinase receptors, leads to HNF1alpha expression, too. These embryonic inducers result in a delayed appearance of HNF1alpha mRNA, excluding a direct activation of HNF1alpha. In contrast, the maternally expressed nuclear receptors HNF4alpha and HNF4beta activate the initial HNF1alpha transcription, since overexpression of HNF4 leads to a rapid expression of HNF1alpha mRNA in animal caps. Similarly, in entire neurulae HNF4 overexpression results in increased HNF1alpha transcription. Therefore, we assume that the initial activation is dependent on maternal HNF4alpha and HNF4beta transcription factors whereas HNF1alpha induction by growth factors reflects the property of these factors to induce the differentiation of mesodermal and entodermal cell types expressing HNF1alpha.