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Published online on February 11, 2008, 10.1073/pnas.0712029105
PNAS | February 19, 2008 | vol. 105 | no. 7 | 2433-2438


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BIOLOGICAL SCIENCES / CELL BIOLOGY
Sterility and absence of histopathological defects in nonreproductive organs of a mouse ERβ-null mutant

Maria Cristina Antal, Andrée Krust, Pierre Chambon*, and Manuel Mark

Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Collège de France, Université Louis Pasteur de Strasbourg, 67404 Illkirch Cedex, France

Contributed by Pierre Chambon, December 21, 2007 (received for review October 7, 2007)

Estrogen signaling is mediated by estrogen receptors {alpha} (ER{alpha}) and β (ERβ). Although a consensus has now been reached concerning many physiological functions of ER{alpha}, those of ERβ are still controversial: When housed and examined in two distant laboratories, mice originating from the same initial ERβ mutant exhibited widely different phenotypes, which were themselves different from the phenotype of another ERβ mutant previously generated in our laboratory. Because, in addition to a knockout insertion in exon 3, all these mouse mutants displayed alternative splicing transcripts, we have now constructed a ERβ mouse mutant (ERβSTL–/L–) in which exon 3 was cleanly deleted by Cre/LoxP-mediated excision and was devoid of any transcript downstream of exon 3. Both females and males were sterile. The histology of the ovary was mildly affected, and no histological defects were detected in other organs, neither in females nor in males. Our present results, which are in contrast with previously published data, suggest that, with the notable exception of male and female reproduction, ERβ is not required in the mouse for the development and homeostasis of the major body systems.

aging | ERβ function | ERβ knockout | estrogen signaling | histopathology


Author contributions: A.K. and M.M. designed research; M.C.A., A.K., and M.M. performed research; M.C.A., A.K., P.C., and M.M. analyzed data; and M.C.A., A.K., P.C., and M.M. wrote the paper.

The authors declare no conflict of interest.

This article contains supporting information online at www.pnas.org/cgi/content/full/0712029105/DC1.

*To whom correspondence should be addressed. E-mail: chambon{at}titus.u-strasbg.fr

© 2008 by The National Academy of Sciences of the USA


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