A maternal epimutation of GNAS leads to Albright osteodystrophy and parathyroid hormone resistance

J Clin Endocrinol Metab. 2008 Mar;93(3):661-5. doi: 10.1210/jc.2007-0927. Epub 2008 Jan 8.

Abstract

Context: Pseudohypoparathyroidism (PHP) type Ia is a rare maternally transmitted disease due to maternal loss-of-function mutations of GNAS, the gene encoding Galphas, the alpha-stimulatory subunit of the G protein. Affected individuals display hormonal resistance (mainly PTH and TSH resistance) and Albright hereditary osteodystrophy. PHP type Ib (PHP-Ib), usually defined by isolated renal resistance to PTH and sometimes mild TSH resistance, is due to a maternal loss of GNAS exon A/B methylation, leading to decreased Galphas expression in specific tissues.

Objective and results: We report a girl with obvious Albright osteodystrophy features, PTH resistance, normal Galphas bioactivity in red blood cells, yet no loss-of-function mutation in the GNAS coding sequence (exons 1-13). The methylation analysis of the four GNAS differentially methylated regions, i.e. NESP, AS, XL, and A/B, revealed broad methylation changes at all differentially methylated regions, including GNAS exon A/B, leading to a paternal epigenotype on both alleles.

Conclusions: This observation suggests that: 1) the decreased expression of Galphas due to GNAS epimutations is not restricted to the renal tubule but may affect nonimprinted tissues like bone; 2) PHP-Ib is a heterogeneous disorder that should lead to studying GNAS epigenotype in patients with PHP and no mutation in GNAS exons 1-13, regardless of their physical features.

MeSH terms

  • Child
  • Chromogranins
  • Epigenesis, Genetic*
  • Female
  • Fibrous Dysplasia, Polyostotic / genetics*
  • GTP-Binding Protein alpha Subunits, Gs / genetics*
  • Humans
  • Mutation*
  • Parathyroid Hormone / physiology*
  • Pseudohypoparathyroidism / genetics*

Substances

  • Chromogranins
  • PTH protein, human
  • Parathyroid Hormone
  • GNAS protein, human
  • GTP-Binding Protein alpha Subunits, Gs