ZFP462 safeguards neural lineage specification by targeting G9A/GLP-mediated heterochromatin to silence enhancers

Nat Cell Biol. 2023 Jan;25(1):42-55. doi: 10.1038/s41556-022-01051-2. Epub 2023 Jan 5.

Abstract

ZNF462 haploinsufficiency is linked to Weiss-Kruszka syndrome, a genetic disorder characterized by neurodevelopmental defects, including autism. Though conserved in vertebrates and essential for embryonic development, the molecular functions of ZNF462 remain unclear. We identified its murine homologue ZFP462 in a screen for mediators of epigenetic gene silencing. Here we show that ZFP462 safeguards neural lineage specification of mouse embryonic stem cells (ESCs) by targeting the H3K9-specific histone methyltransferase complex G9A/GLP to silence meso-endodermal genes. ZFP462 binds to transposable elements that are potential enhancers harbouring pluripotency and meso-endoderm transcription factor binding sites. Recruiting G9A/GLP, ZFP462 seeds heterochromatin, restricting transcription factor binding. Loss of ZFP462 in ESCs results in increased chromatin accessibility at target sites and ectopic expression of meso-endodermal genes. Taken together, ZFP462 confers lineage and locus specificity to the broadly expressed epigenetic regulator G9A/GLP. Our results suggest that aberrant activation of lineage non-specific genes in the neuronal lineage underlies ZNF462-associated neurodevelopmental pathology.

MeSH terms

  • Animals
  • Chromatin
  • DNA-Binding Proteins / genetics
  • Embryonic Stem Cells
  • Heterochromatin* / genetics
  • Histone-Lysine N-Methyltransferase* / genetics
  • Histone-Lysine N-Methyltransferase* / metabolism
  • Mice
  • Nerve Tissue Proteins / genetics
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • Heterochromatin
  • Histone-Lysine N-Methyltransferase
  • Chromatin
  • Transcription Factors
  • Zfp462 protein, mouse
  • DNA-Binding Proteins
  • Nerve Tissue Proteins