Open AccessSterility and absence of histopathological defects in nonreproductive organs of a mouse ERβ-null mutant
Author(s) -
Maria Cristina Antal,
Andrée Krust,
Pierre Chambon,
Manuel Mark
Publication year - 2008
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0712029105
Subject(s) - mutant , biology , exon , phenotype , sterility , knockout mouse , estrogen receptor , alternative splicing , microbiology and biotechnology , null allele , estrogen , genetics , medicine , endocrinology , receptor , gene , cancer , breast cancer
Estrogen signaling is mediated by estrogen receptors alpha (ERalpha) and beta (ERbeta). Although a consensus has now been reached concerning many physiological functions of ERalpha, those of ERbeta are still controversial: When housed and examined in two distant laboratories, mice originating from the same initial ERbeta mutant exhibited widely different phenotypes, which were themselves different from the phenotype of another ERbeta 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 ERbeta mouse mutant (ERbeta(ST)(L-/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, ERbeta is not required in the mouse for the development and homeostasis of the major body systems.