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# 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
Proceedings of the National Academy of Sciences of the United States of America
Vol. 105, No. 7 (Feb. 19, 2008), pp. 2433-2438
Stable URL: http://www.jstor.org/stable/25451484
Page Count: 6
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## Abstract

Estrogen signaling is mediated by estrogen receptors a (ERα) and β (ERβ). Although a consensus has now been reached concerning many physiological functions of ERα, 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 $({\rm ER}\beta _{{\rm ST}}{}^{{\rm L}-/{\rm L}-})$ 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.

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