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Abstract
Mice lacking neuroD2, a basic helix-loop-helix transcription factor involved in brain development, show growth retardation and other abnormalities consistent with hypothalamic-pituitary-thyroid (HPT) axis dysfunction. neuroD2 is expressed in the paraventricular hypothalamic nuclei, the anterior lobe of pituitary, and the thyroid gland. In neuroD2-deficient mice, thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormone are decreased in these three regions, respectively. neuroD2-null mice typically die 2 to 3 weeks after birth, but those treated with replacement doses of thyroxine survived more than 8 weeks. These data indicate that neuroD2 is expressed throughout the HPT axis and that all levels of the axis are functionally affected by its absence in mice.
We thank Matthew Fero and Wei-Ming Chien for technical advice and critical discussion and Gad Kletter for helpful comments on the manuscript.
This project was supported by NIH grants AR45113 and NS36086 to S.J.T. and by the Burroughs Wellcome Career Award in Biomedical Science and institutional startup funds to J.M.O.