Two sides of the Dlk1-Dio3 story in imprinting

Yee Hoon Foong; Joanne L Thorvaldsen; Marisa S Bartolomei

doi:10.1016/j.devcel.2021.10.021

Two sides of the Dlk1-Dio3 story in imprinting

Dev Cell. 2021 Nov 22;56(22):3035-3037. doi: 10.1016/j.devcel.2021.10.021.

Authors

Yee Hoon Foong¹, Joanne L Thorvaldsen¹, Marisa S Bartolomei²

Affiliations

¹ Epigenetics Institute, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
² Epigenetics Institute, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: bartolom@pennmedicine.upenn.edu.

PMID: 34813763
DOI: 10.1016/j.devcel.2021.10.021

Abstract

Loss of imprinting (LOI) at the Dlk1-Dio3 locus is linked to Kagami-Ogata and Temple syndromes, and to cancer, but molecular mechanisms that prevent LOI are under-studied. In this issue of Developmental Cell, Aronson et al. demarcate the bipartite regulation of the Dlk1-Dio3 imprinting control region (ICR) IG-DMR, which maintains locus imprinting.

Publication types

Comment

MeSH terms

Calcium-Binding Proteins / genetics
DNA Methylation
Genomic Imprinting*
Humans
Membrane Proteins / genetics
Neoplasms*

Substances

Calcium-Binding Proteins
DLK1 protein, human
Membrane Proteins