RRC ID 88292
Author Su L, Xia W, Shen T, Liang Q, Wang W, Li H, Jiao J.
Title H2A.Z.1 crosstalk with H3K56-acetylation controls gliogenesis through the transcription of folate receptor.
Journal Nucleic Acids Res
Abstract Astrocytes play crucial roles in the central nervous system, and defects in astrocyte function are closely related to many neurological disorders. Studying the mechanism of gliogenesis has important implications for understanding and treating brain diseases. Epigenetic regulations have essential roles during mammalian brain development. Here, we demonstrate that histone H2A.Z.1 is necessary for the specification of multiple neural precursor cells (NPCs) and has specialized functions that regulate gliogenesis. Depletion of H2A.Z.1 suppresses gliogenesis and results in reduced astrocyte differentiation. Additionally, H2A.Z.1 regulates the acetylation of H3K56 (H3K56ac) by cooperating with the chaperone of ASF1a. Furthermore, RNA-seq data indicate that folate receptor 1 (FOLR1) participates in gliogenesis through the JAK-STAT signaling pathway. Taken together, our results demonstrate that H2A.Z.1 is a key regulator of gliogenesis because it interacts with ASF1a to regulate H3K56ac and then directly affects the expression of FOLR1, which acts as a signal-transducing component of the JAK-STAT signaling pathway.
Volume 46(17)
Pages 8817-8831
Published 2018-9-28
DOI 10.1093/nar/gky585
PII 5048032
PMID 29982651
PMC PMC6158499
MeSH Acetylation Animals Astrocytes / physiology Cell Cycle Proteins Cells, Cultured Chromosomal Proteins, Non-Histone / metabolism Embryo, Mammalian Female Folate Receptor 1 / genetics* Gene Expression Regulation, Developmental HEK293 Cells Histone Acetyltransferases / metabolism* Histones / metabolism* Histones / physiology Humans Male Mice Mice, Inbred C57BL Mice, Inbred ICR Mice, Transgenic Molecular Chaperones Neural Stem Cells Neurogenesis / genetics* Neuroglia / physiology* Pregnancy Signal Transduction / genetics Transcription, Genetic
IF 11.502
Resource
Mice RBRC05765