期刊
ENDOCRINOLOGY
卷 163, 期 11, 页码 -出版社
ENDOCRINE SOC
DOI: 10.1210/endocr/bqac131
关键词
transcription; inhibin; receptor; pituitary; knockout mouse; cell line
资金
- Canadian Institutes of Health Research [PJT-162343]
- National Institutes of Health [DK46943]
- Medical Research Council (M.R.C.) [MR/T012153/1]
- McGill University Health Centre
- Canadian Institutes of Health Research
- Fonds de Recherche du Quebec - Sante
- Cell Therapies and Regenerative Medicine Four-Year Welcome Trust PhD Training Programme (King's College London)
Inhibins control reproduction by suppressing follicle-stimulating hormone synthesis, and SF-1 directly regulates the transcription of Tgfbr3l/TGFBR3L, playing a role in gonadotrope cells.
The inhibins control reproduction by suppressing follicle-stimulating hormone synthesis in pituitary gonadotrope cells. The newly discovered inhibin B coreceptor, TGFBR3L, is selectively and highly expressed in gonadotropes in both mice and humans. Here, we describe our initial characterization of mechanisms controlling cell-specific Tgfbr3l/TGFBR3L transcription. We identified two steroidogenic factor 1 (SF-1 or NR5A1) cis-elements in the proximal Tgfbr3l promoter in mice. SF-1 induction of murine Tgfbr3l promoter-reporter activity was inhibited by mutations in one or both sites in heterologous cells. In homologous cells, mutation of these cis-elements or depletion of endogenous SF-1 similarly decreased reporter activity. We observed nearly identical results when using a human TGFBR3L promoter-reporter. The Tgfbr3l gene was tightly compacted and Tgfbr3l mRNA expression was essentially absent in gonadotropes of SF-1 (Nr5a1) conditional knockout mice. During murine embryonic development, Tgfbr3l precedes Nr5a1 expression, though the two transcripts are fully colocalized by embryonic day 18.5 and thereafter. Collectively, these data indicate that SF-1 directly regulates Tgfbr3l/TGFBR3L transcription and is required for postnatal expression of the gene in gonadotropes.
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