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First published online 17 July 2008
doi: 10.1242/dev.023010

Development 135, 2777-2786 (2008)
Published by The Company of Biologists 2008
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Crucial role of vHNF1 in vertebrate hepatic specification

Ludmilla Lokmane, Cécile Haumaitre*, Pilar Garcia-Villalba{dagger}, Isabelle Anselme, Sylvie Schneider-Maunoury and Silvia Cereghini{ddagger}

Centre National de la Recherche Scientifique, UMR7622 Biologie du Developpement, 9 quai St. Bernard Bât. C, 75005 Paris, France and Université Pierre et Marie Curie, UMR7622 Developmental Biology, 9 quai St. Bernard Bât. C, 75005 Paris, France.

{ddagger} Author for correspondence (e-mail: silvia.cereghini{at}snv.jussieu.fr)

Accepted 19 June 2008

Mouse liver induction occurs via the acquisition of ventral endoderm competence to respond to inductive signals from adjacent mesoderm, followed by hepatic specification. Little is known about the regulatory circuit involved in these processes. Through the analysis of vHnf1 (Hnf1b)-deficient embryos, generated by tetraploid embryo complementation, we demonstrate that lack of vHNF1 leads to defective hepatic bud formation and abnormal gut regionalization. Thickening of the ventral hepatic endoderm and expression of known hepatic genes do not occur. At earlier stages, hepatic specification of vHnf1-/- ventral endoderm is disrupted. More importantly, mutant ventral endoderm cultured in vitro loses its responsiveness to inductive FGF signals and fails to induce the hepatic-specification genes albumin and transthyretin. Analysis of liver induction in zebrafish indicates a conserved role of vHNF1 in vertebrates. Our results reveal the crucial role of vHNF1 at the earliest steps of liver induction: the acquisition of endoderm competence and the hepatic specification.

Key words: Liver specification, vHNF1 (HNF1β, TCF2), Mouse, Zebrafish


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