Dependence of fertility on kisspeptin-Gpr54 signaling at the GnRH neuron
Signaling between kisspeptin and its receptor, G-protein-coupled receptor 54 (Gpr54), is now recognized as being essential for normal fertility. However, the key cellular location of kisspeptin-Gpr54 signaling is unknown. Here we create a mouse with a GnRH neuron-specific deletion of Gpr54 to assess...
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| Main Authors: | , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
20 Sep 2013
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| In: |
Nature Communications
Year: 2013, Volume: 4, Pages: 1-11 |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/ncomms3492 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/ncomms3492 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/ncomms3492 
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| Author Notes: | Milen Kirilov, Jenny Clarkson, Xinhuai Liu, Juan Roa, Pauline Campos, Rob Porteous, Günther Schütz & Allan E. Herbison |
MARC
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| 520 | |a Signaling between kisspeptin and its receptor, G-protein-coupled receptor 54 (Gpr54), is now recognized as being essential for normal fertility. However, the key cellular location of kisspeptin-Gpr54 signaling is unknown. Here we create a mouse with a GnRH neuron-specific deletion of Gpr54 to assess the role of gonadotropin-releasing hormone (GnRH) neurons. Mutant mice are infertile, fail to go through puberty and exhibit markedly reduced gonadal size and follicle-stimulating hormone levels alongside GnRH neurons that are unresponsive to kisspeptin. In an attempt to rescue the infertile phenotype of global Gpr54−/− mutants, we use BAC transgenesis to target Gpr54 to the GnRH neurons. This results in mice with normal puberty onset, estrous cyclicity, fecundity and a recovery of kisspeptin’s stimulatory action upon GnRH neurons. Using complimentary cell-specific knockout and knockin approaches we demonstrate here that the GnRH neuron is the key site of kisspeptin-Gpr54 signaling for fertility. | ||
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