ArticleMolecular and cellular biology1995
The POU homeodomain transcription factor Oct-1 is essential for activity of the gonadotropin-releasing hormone neuron-specific enhancer.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 122 citations in OpenAlex.
- Leukemia Inhibitory Factor Represses GnRH Gene Expression via cFOS during Inflammation in Male Mice.Neuroendocrinology · 2019Article
- The Arcuate Estrogen-Regulated Transcriptome: Estrogen Response Element-Dependent and -Independent Signaling of ERα in Female Mice.Endocrinology · 2017Article
- Article
- The POU factor ventral veins lacking/Drifter directs the timing of metamorphosis through ecdysteroid and juvenile hormone signaling.PLoS genetics · 2014Article
- Neurokinin B causes acute GnRH secretion and repression of GnRH transcription in GT1-7 GnRH neurons.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Epigenetic control of gonadotropin releasing hormone neurons.Frontiers in endocrinology · 2013Article
- Ultra-rare mutation in long-range enhancer predisposes to thyroid carcinoma with high penetrance.PloS one · 2013Article
- Androgen receptor repression of gonadotropin-releasing hormone gene transcription via enhancer 1.Molecular and cellular endocrinology · 2012Article
- Androgen receptor repression of GnRH gene transcription.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Class-C SOX transcription factors control GnRH gene expression via the intronic transcriptional enhancer.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Identification of a dopaminergic enhancer indicates complexity in vertebrate dopamine neuron phenotype specification.Developmental biology · 2011Article
- The gonadotropin-releasing hormone cell-specific element is required for normal puberty and estrous cyclicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Dynamic chromatin modifications control GnRH gene expression during neuronal differentiation and protein kinase C signal transduction.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Hypothalamic dysregulation and infertility in mice lacking the homeodomain protein Six6.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Epigenetic changes coincide with in vitro primate GnRH neuronal maturation.Endocrinology · 2010Article
- Enhancers of GnRH transcription embedded in an upstream gene use homeodomain proteins to specify hypothalamic expression.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Regulation of gonadotropin-releasing hormone-1 gene transcription by members of the purine-rich element-binding protein family.American journal of physiology. Endocrinology and metabolism · 2010Article
- GnRH pulsatility, the pituitary response and reproductive dysfunction.Endocrine journal · 2009Review
- Heterogeneous nuclear ribonucleoprotein A/B and G inhibits the transcription of gonadotropin-releasing-hormone 1.Molecular and cellular neurosciences · 2008Article
- Mammalian comparative sequence analysis of the Agrp locus.PloS one · 2007Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms of specification of gene expression in a complex tissue such as the brain remain poorly understood. To provide a model system for the study of gene regulation in a specific subpopulation of differentiated neurons, we have derived cell lines from tumors created in transgenic mice by targeting simian virus 40 T antigen expression by using the regulatory regions of the gene for gonadotropin-releasing hormone (GnRH), a decapeptide released from specialized neurons in the hypothalamus. Transfections into the cultured GnRH-secreting hypothalamic neuronal cell line GT1 have identified a neuron-specific enhancer, 1.5 kb upstream of the GnRH gene, which binds multiple GT1 nuclear proteins. In particular, one AT-rich protein-binding region, AT-a, is critical for enhancer activity. In this study, we used electrophoretic mobility shift assays to detect a GT1 nuclear protein complex that binds the AT-a region. Close inspection of the AT-a bottom-strand sequence revealed homology to the octamer motif, a sequence known to bind members of the POU homeodomain transcription factor family. Although we demonstrate expression of a number of POU homeodomain genes in GT1 cells, a supershift assay with Oct-1 antibody demonstrates that Oct-1 is the protein binding the enhancer. Finally, specific mutations in the AT-a region that affected Oct-1 binding were correlated with decreased transcription. Thus, Oct-1 binds to the GnRH enhancer in vitro, and this binding is critical to the transcriptional activity of this neuron-specific enhancer in GT1 cells.
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