The origin of imprinting defects in Temple syndrome and comparison with other imprinting disorders

Epigenetics. 2018;13(8):822-828. doi: 10.1080/15592294.2018.1514233. Epub 2018 Sep 19.

Abstract

Temple syndrome (TS14) is a rare imprinting disorder caused by genetic and epigenetic alterations on chromosome 14q32. A subset of these patients shows an imprinting defect (ID) where the paternal allele harbors a maternal epigenotype thus silencing the paternally expressed genes and leading to an increased expression of the maternally expressed genes. We investigated the grandparental origin of the incorrectly imprinted chromosome 14 in a cohort of 13 TS14 ID patients and their families. In seven families grandmaternal and, in six families, grandpaternal inheritance was observed. These results indicate that the ID occurred after imprint erasure in the paternal germ line. While the complete lack of methylation as observed in the majority of TS14 ID patients may be due to an imprint establishment error in the paternal germ line, cases with methylation mosaicism suggest that in general many IDs (TS14, AS, BWS, and SRS) are in fact of somatic origin in the early or late embryo.

Keywords: Temple syndrome; genomic imprinting; imprint establishment; methylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abnormalities, Multiple / genetics*
  • Adult
  • Aged
  • Child
  • Chromosomes, Human, Pair 14 / genetics*
  • DNA Methylation*
  • Female
  • Genomic Imprinting*
  • Germ Cells / metabolism
  • Grandparents
  • Humans
  • Male
  • Middle Aged
  • Muscle Hypotonia / genetics*
  • Obesity / genetics*
  • Pedigree
  • Syndrome

Grants and funding

This work was funded by the Bundesministerium für Bildung und Forschung (BMBF; Imprinting diseases, grant No. 01GM1513A and D).