PUBLICATION
G9a and ZNF644 Physically Associate to Suppress Progenitor Gene Expression during Neurogenesis
- Authors
- Olsen, J.B., Wong, L., Deimling, S., Miles, A., Guo, H., Li, Y., Zhang, Z., Greenblatt, J.F., Emili, A., Tropepe, V.
- ID
- ZDB-PUB-160823-4
- Date
- 2016
- Source
- Stem Cell Reports 7(3): 454-70 (Journal)
- Registered Authors
- Li, Yue, Tropepe, Vincent, Wong, Loksum
- Keywords
- none
- Datasets
- GEO:GSE63225
- MeSH Terms
-
- Retina/metabolism
- Gene Expression Regulation, Developmental*
- Histones/metabolism
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- PubMed
- 27546533 Full text @ Stem Cell Reports
Abstract
Proliferating progenitor cells undergo changes in competence to give rise to post-mitotic progeny of specialized function. These cell-fate transitions typically involve dynamic regulation of gene expression by histone methyltransferase (HMT) complexes. However, the composition, roles, and regulation of these assemblies in regulating cell-fate decisions in vivo are poorly understood. Using unbiased affinity purification and mass spectrometry, we identified the uncharacterized C2H2-like zinc finger protein ZNF644 as a G9a/GLP-interacting protein and co-regulator of histone methylation. In zebrafish, functional characterization of ZNF644 orthologs, znf644a and znf644b, revealed complementary roles in regulating G9a/H3K9me2-mediated gene silencing during neurogenesis. The non-overlapping requirements for znf644a and znf644b during retinal differentiation demarcate critical aspects of retinal differentiation programs regulated by differential G9a-ZNF644 associations, such as transitioning proliferating progenitor cells toward differentiation. Collectively, our data point to ZNF644 as a critical co-regulator of G9a/H3K9me2-mediated gene silencing during neuronal differentiation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping