Gonadal effects of a mouse Denys-Drash syndrome mutation.
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| Grant Information: | MC_U127661055 United Kingdom MRC_ Medical Research Council; U.1276.00.002(61055) United Kingdom MRC_ Medical Research Council |
| Substance Nomenclature: | 0 (Glycoproteins) 0 (Receptors, Androgen) 0 (Testicular Hormones) 0 (WT1 Proteins) 80497-65-0 (Anti-Mullerian Hormone) |
| Entry Date(s): | Date Created: 20051026 Date Completed: 20060125 Latest Revision: 20220129 |
| Update Code: | 20231215 |
| DOI: | 10.1007/s11248-005-7216-y |
| PMID: | 16245160 |
| Autor: | Patek CE; Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, Western General Hospital, Crewe Road, EH4 2XU Edinburgh, UK., Saunders PT, Miles CG, Berry RL, Hastie ND, Sharpe RM, Hooper ML |
| Jazyk: | angličtina |
| Zdroj: | Transgenic research [Transgenic Res] 2005 Oct; Vol. 14 (5), pp. 691-702. |
| DOI: | 10.1007/s11248-005-7216-y |
| Abstrakt: | Gonadal effects of the Denys-Drash syndrome (DDS) mutation Wt1(tmT396 )were examined in chimaeric and heterozygous mice. Since the only heterozygote was 41,XXY, Sertoli cell function was assessed by comparison with age-matched control XXY testes. Control XXY Sertoli cells showed immuno-expression of WT1 and androgen receptor (AR) indistinguishable from wild-type (40,XY), but expressed anti-Mullerian hormone (AMH). In contrast, DDS Sertoli cells showed only faint immuno-expression of WT1 and did not express AR or AMH. While XY<-->XY DDS chimaeras were male, XX<-->XY chimaeras were predominantly female. In the rare XX<-->XY DDS males the Sertoli cell lineage was largely derived from Wt1 mutant XY cells. We conclude that DDS mutant cells can form Sertoli cells, that the dominant mutation does not cause male sex reversal in mice but distorts the sex ratio of XX<-->XY chimaeras, and that there may be a link between WT1, AMH and AR expression by Sertoli cells in vivo. |
| Databáze: | MEDLINE |
| Externí odkaz: |
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