MON-041 - Loss of Primary Cilia in Late Pituitary Organogenesis Does Not Cause Endocrine Dysfunction

Cilia are finger-like organelles protruding from the cell membrane, and dysfunction of cilia can cause human diseases called ciliopathies with a range of phenotypes. Some ciliopathies include pituitary phenotypes, and previous studies have shown a role for non-motile primary cilia in pituitary organogenesis.
In this study, we generated a pituitary gland-conditional knockout of the ciliary basal body protein CEP164 to investigate the role of primary cilia in pituitary development and postnatal function. While Prop1-Cre causes recombination throughout the pituitary gland by e12.5, Prop1-Cre; Cep164f/f embryos show a loss of pituitary primary cilia between e14.5 and e18.5. Pituitary organogenesis and morphology appear normal in late embryos and postpubertal mice of both sexes despite the loss of primary cilia from after initial pituitary organogenesis. No physiological defects were noted in postpubertal mice, although there were minor changes in expression of Sox2 and Prl transcripts by quantitative PCR. Localization of SOX2 by immunofluorescence was normal along the pituitary cleft.
Together with other studies that have demonstrated pituitary defects in embryos with early loss or dysfunction of cilia, we conclude that primary cilia are dispensable in late pituitary organogenesis, therefore suggesting the role of primary cilia occur during early pituitary development. Further studies may investigate whether cilia are required for specific responses to physiological or pathological conditions where endocrine needs are altered.

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