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Submitted on May 17, 2002
Accepted on February 28, 2003
1 Molecular Endocrinology, INSERM Unit 344, Faculté de Médecine Necker-Enfants Malades Paris, France (N. B., P. I. B., N. B., P. A. K.), Unité de Différenciation Cellulaire, INRA, Jouy en Josas, France (C. V.)
* To whom correspondence should be addressed. E-mail: binart{at}necker.fr.
The heterozygous PRL receptor (PRLR +/-) mouse fails to develop a fully functional mammary gland at the end of the first pregnancy and shows markedly impaired lobuloalveolar development and milk secretion in young females. The PRL receptor is expressed ubiquitously, with various proportions of long and short isoforms in different tissues. Conflicting data have appeared on the putative role of the receptor short forms with both agonist and antagonistic actions proposed. To assess whether the mouse PR-1 short isoform of the PRL receptor is potentially able to transduce a signal, we overexpressed it in heterozygous mice and investigated its effect on the rescue of mammary development. PRLR+/- mice were not able to develop a functional mammary gland, but restoration of mammary alveolar development and an increase in the expressions of casein and WAP genes were observed in transgenic PRLR+/- mice expressing the short form of the PRLR, leading to a complete rescue of mammary gland development and function in young females. These results demonstrate that PR-1 the short form of the PRLR can improve mammary development in PRLR+/- mice compensating the haploinsufficiency of the receptor long form, the effect probably being due to accelerated proliferation and an activation of the PRLR signaling cascade, resulting in activation of target genes involved in mammary development and milk synthesis.
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