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First published online 26 January 2005
doi: 10.1242/dev.01648
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receptor is necessary for implementation of erythropoiesis in the neonatal spleen environment in the mouse
1 Laboratory of Molecular Cell Biology, Ecole Normale Supérieure de Lyon,
UMR CNRS 5161, INRA 1237, IFR128 Biosciences Lyon-Gerland, 46 Allée
d'Italie, 69364 Lyon Cedex 07, France
2 Department of Gynecologic Endocrinology and Reproductive Medicine, Medical
University of Vienna, Vienna, Austria
3 Research Institute of Molecular Pathology (IMP), Dr Bohr Gasse 7, 1030 Vienna,
Austria
4 Université Claude Bernard Lyon I, 43 bd du 11 Novembre 1918, 69622
Villeurbanne cedex, France
* Author for correspondence (e-mail: jacques.samarut{at}ens-lyon.fr)
Accepted 16 December 2004
Thyroid hormones (THs) mediate many physiological and developmental
functions in vertebrates. All these functions are mediated by binding of the
active form of the TH T3 to the specific nuclear receptors TR
and
TRß, which are transcription factors. Using mutant mice lacking TRs or
deficient for TH production, we show that T3 influences neonatal
erythropoiesis through TR. The effect of T3 and TR is restricted
to this developmental window and is specific for the spleen but not for other
erythropoietic organs. We show that T3 via TR affects late steps of
erythrocytic development, promoting the proliferation of late basophilic
erythroblasts. In vitro, this effect is exerted directly on erythrocytic
cells. In vivo, the action of T3 is also intrinsic to spleen erythrocytic
progenitors, as shown by grafting experiments of splenocytes derived from
wildtype and TR knockout (TR0/0) mice into wild-type
and TR0/0 irradiated recipients. Our results indicate that
defective spleen erythropoiesis in hypothyroid and TR0/0
mice results from impaired recognition of the spleen environment by the mutant
erythrocytic progenitors. The data presented support a model in which T3
signaling through TR is essential for the implementation of the
transient spleen erythropoiesis at birth.
Key words: Thyroid hormone, Nuclear receptor, Erythropoiesis, Mouse
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