| First Author | Maneix L | Year | 2015 |
| Journal | Proc Natl Acad Sci U S A | Volume | 112 |
| Issue | 16 | Pages | 5135-40 |
| PubMed ID | 25848008 | Mgi Jnum | J:220968 |
| Mgi Id | MGI:5637603 | Doi | 10.1073/pnas.1504944112 |
| Citation | Maneix L, et al. (2015) Estrogen receptor beta exon 3-deleted mouse: The importance of non-ERE pathways in ERbeta signaling. Proc Natl Acad Sci U S A 112(16):5135-40 |
| abstractText | In 1998, an estrogen receptor beta (ERbeta) knockout (KO) mouse was created by interrupting the gene at the DNA binding domain (DBD) with a neocassette. The mutant females were subfertile and there were abnormalities in the brain, prostate, lung, colon, and immune system. In 2008, another ERbeta mutant mouse was generated by deleting ERbeta exon 3 which encodes the first zinc finger in the DBD. The female mice of this strain were unable to ovulate but were otherwise normal. The differences in the phenotypes of the two KO strains, have led to questions about the physiological function of ERbeta. In the present study, we created an ERbeta exon 3-deleted mouse (ERbeta-Deltaex3) and confirmed that the only observable defect was anovulation. Despite the two in-frame stop codons introduced by splicing between exons 2 and 4, an ERbeta protein was expressed in nuclei of prostate epithelial cells. Using two different anti-ERbeta antibodies, we showed that an in-frame ligand binding domain and C terminus were present in the ERbeta-Deltaex3 protein. Moreover, with nuclear extracts from ERbeta-Deltaex3 prostates, there was an ERbeta-dependent retardation of migration of activator protein-1 response elements in EMSA. Unlike the original knockout mouse, expression of Ki67, androgen receptor, and Dachshund-1 in prostate epithelium was not altered in the ERbeta-Deltaex3 mouse. We conclude that very little of ERbeta transcriptional activity depends on binding to classical estrogen response elements (EREs). |
