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Molecular and Cellular Biology, July 2001, p. 4761-4772, Vol. 21, No. 14
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.14.4761-4772.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Functional Interference between Thyroid Hormone Receptor alpha  (TRalpha ) and Natural Truncated TRDelta alpha Isoforms in the Control of Intestine Development

Michelina Plateroti,1 Karine Gauthier,1 Claire Domon-Dell,2 Jean-Noël Freund,2 Jacques Samarut,1,* and Olivier Chassande1

Laboratoire de Biologie Moléculaire et Cellulaire de l'ENS de Lyon, UMR 5665 CNRS, LA 913 INRA, 69364 Lyon Cedex 07,1 and INSERM U.381, 67200 Strasbourg,2 France

Received 27 November 2000/Returned for modification 13 February 2001/Accepted 15 April 2001

Thyroid hormone is known to participate in the control of intestine maturation at weaning. Its action is mediated by the thyroid hormone nuclear receptors, encoded by the TRalpha and TRbeta genes. Since previous studies have shown that TRbeta plays a minor role in the gut, we focused here our analysis on the TRalpha gene. The TRalpha locus generates the TRalpha 1 receptor together with the splicing variant TRalpha 2 and the truncated products TRDelta alpha 1 and TRDelta alpha 2, which all lack an intact ligand binding domain. The TRDelta alpha isoforms are transcribed from an internal promoter located in intron 7, and their distribution is restricted to a few tissues including those of the intestine. In order to define the functions of the different isoforms encoded by the TRalpha locus in the intestinal mucosa, we produced mice either lacking all known TRalpha products or harboring a mutation which inactivates the intronic promoter. We performed a detailed analysis of the intestinal phenotypes in these mice and compared it to that of the previously described TRalpha -/- mice, in which TRalpha isoforms are abolished but the TRDelta alpha isoforms remain. This comparative analysis leads us to the following conclusions: (i) the TRalpha 1 receptor mediates the T3-dependent functions in the intestine at weaning time and (ii) the TRDelta alpha products negatively control the responsiveness of the epithelial cells to T3. Moreover, we show that TRDelta alpha proteins can interfere with the transcription of the intestine-specific homeobox genes cdx1 and cdx2 and that their activity is regulated by TRalpha 1. Altogether these data demonstrate that cooperation of TRalpha and TRDelta alpha products is essential to ensure the normal postnatal development of the intestine and that mutations in the TRalpha locus can generate different phenotypes caused by the disruption of the equilibrium between these products.

* Corresponding author. Mailing address: Laboratoire de Biologie Moléculaire et Cellulaire de l'ENS de Lyon, UMR 5665 CNRS, LA 913 INRA, 46 allée d'Italie, 69364 Lyon Cedex 07, France. Phone: 33 4 72 72 81 71. Fax: 33 4 72 72 85 36. E-mail: Jacques.Samarut{at}ens-lyon.Fr.

Molecular and Cellular Biology, July 2001, p. 4761-4772, Vol. 21, No. 14
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.14.4761-4772.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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