Mutations in PROP1 cause familial combined pituitary hormone deficiency (original) (raw)
- Letter
- Published: 01 February 1998
- Joy D. Cogan2,
- Roland W. Pfäffle3,
- Jeremy S. Dasen1,
- Herwig Frisch4,
- Shawn M. O'Connell1,
- Sarah E. Flynn1,
- Milton R. Brown5,
- Primus E. Mullis6,
- John S. Parks5,
- John A. Phillips III2 &
- …
- Michael G. Rosenfeld1
Nature Genetics volume 18, pages 147–149 (1998)Cite this article
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Abstract
Combined pituitary hormone deficiency (CPHD) in man denotes impaired production of growth hormone (GH) and one or more of the other five anterior pituitary hormones. Mutations of the pituitary transcription factor gene POU1F1 (the human homologue of mouse Pit1) are responsible for deficiencies of GH, prolactin and thyroid stimulating hormone (TSH) in Snell and Jackson dwarf mice and in man, while the production of adrenocorticotrophic hormone (ACTH), luteiniz-ing hormone (LH) and follicle stimulating hormone (FSH) is preserved. The Ames dwarf (df) mouse displays a similar phenotype, and appears to be epistatic to Snell and Jackson dwarfism. We have recently positionally cloned the putative Ames dwarf gene Prop1 (ref. 1)f which encodes a paired-like homeodomain protein that is expressed specifically in embryonic pituitary and is necessary for Pit1 expression. In this report we have identified four CPHD families with homozy-gosity or compound heterozygosity for inactivating mutations of PROP1. These mutations in the human PROP1 gene result in a gene product with reduced DNA-binding and transcriptional activation ability in comparison to the product of the murine df mutation. In contrast to individuals with POU1F1 mutations, those with PROP1 mutations cannot produce LH and FSH at a sufficient level and do not enter puberty spontaneously. Our results identify a major cause of CPHD in humans and suggest a direct or indirect role for PROP1 in the ontogenesis of pituitary gonadotropes, as well as somatotropes, lactotropes and caudomedial thyrotropes.
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Authors and Affiliations
- Howard Hughes Medical Institute, University of California at San Diego, Lajolla, California, 92093-0648, USA
Wei Wu, Jeremy S. Dasen, Shawn M. O'Connell, Sarah E. Flynn & Michael G. Rosenfeld - Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee, 37232, USA
Joy D. Cogan & John A. Phillips III - Department of Pediatrics, RWTH Aachen School of Medicine, 52057, Aachen, Germany
Roland W. Pfäffle - Division of Endocrinology, Department of Pediatrics, University of Vienna, 1090, Wien, Austria
Herwig Frisch - Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia, 30322, USA
Milton R. Brown & John S. Parks - Division of Endocrinology, Department of Pediatrics, University of Bern, Inselspital, CH-3010, Bern, Switzerland
Primus E. Mullis
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Wu, W., Cogan, J., Pfäffle, R. et al. Mutations in _PROP_1 cause familial combined pituitary hormone deficiency.Nat Genet 18, 147–149 (1998). https://doi.org/10.1038/ng0298-147
- Received: 14 October 1997
- Accepted: 22 December 1997
- Issue Date: 01 February 1998
- DOI: https://doi.org/10.1038/ng0298-147