» Articles » PMID: 28588451

Neurogenic to Gliogenic Fate Transition Perturbed by Loss of HMGB2

Overview
Specialty Molecular Biology
Date 2017 Jun 8
PMID 28588451
Citations 11
Authors
Affiliations
Soon will be listed here.
Abstract

Mouse cortical development relies heavily on a delicate balance between neurogenesis and gliogenesis. The lateral ventricular zone produces different classes of excitatory pyramidal cells until just before birth, when the production of astroglia begins to prevail. Epigenetic control of this fate shift is of critical importance and chromatin regulatory elements driving neuronal or astroglial development play an vital role. Different classes of chromatin binding proteins orchestrate the transcriptional repression of neuronal-specific genes, while allowing for the activation of astrocyte-specific genes. Through proteomic analysis of embryonic neural progenitor cells (NPCs) our group had previously identified high mobility group B2 (HMGB2), a chromatin protein dynamically expressed throughout embryonic development. In the current study using cultures of perinatal NPCs from HMGB2 and HMGB2 mice we discovered that vital elements of the polycomb group (PcG) epigenetic complexes polycomb repressive complexes 1 and 2 (PRC1/2) were downregulated during the differentiation process of HMGB2-null NPCs. These epigenetic changes led to downstream changes in specific histone modification levels, specifically the trimethylation of H3K27, and a subsequent shift in the perinatal neurogenesis to gliogenesis fate transition. Collectively these results demonstrate that chromatin binding proteins, such as HMGB2, can have significant effects on the epigenetic landscape of perinatal neural stem/progenitor cells.

Citing Articles

Longitudinal scRNA-seq analysis in mouse and human informs optimization of rapid mouse astrocyte differentiation protocols.

Frazel P, Labib D, Fisher T, Brosh R, Pirjanian N, Marchildon A Nat Neurosci. 2023; 26(10):1726-1738.

PMID: 37697111 PMC: 10763608. DOI: 10.1038/s41593-023-01424-2.


SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development.

Matsui Y, Djekidel M, Lindsay K, Samir P, Connolly N, Wu G Nat Commun. 2023; 14(1):4754.

PMID: 37553330 PMC: 10409800. DOI: 10.1038/s41467-023-40487-4.


Stepwise fate conversion of supporting cells to sensory hair cells in the chick auditory epithelium.

Matsunaga M, Yamamoto R, Kita T, Ohnishi H, Yamamoto N, Okano T iScience. 2023; 26(2):106046.

PMID: 36818302 PMC: 9932131. DOI: 10.1016/j.isci.2023.106046.


HMGA2 Promotes Brain Injury in Rats with Cerebral Infarction by Activating TLR4/NF-B Signaling Pathway.

Huang S, Hong Z, Zhang L, Guo J, Li Y, Li K Mediators Inflamm. 2022; 2022:1376959.

PMID: 35966335 PMC: 9371803. DOI: 10.1155/2022/1376959.


Putative Roles of SETBP1 Dosage on the SET Oncogene to Affect Brain Development.

Antonyan L, Ernst C Front Neurosci. 2022; 16:813430.

PMID: 35685777 PMC: 9173722. DOI: 10.3389/fnins.2022.813430.


References
1.
Steelman A, Zhou Y, Koito H, Kim S, Payne H, Lu Q . Activation of oligodendroglial Stat3 is required for efficient remyelination. Neurobiol Dis. 2016; 91:336-46. PMC: 4962532. DOI: 10.1016/j.nbd.2016.03.023. View

2.
Shechter D, Dormann H, Allis C, Hake S . Extraction, purification and analysis of histones. Nat Protoc. 2007; 2(6):1445-57. DOI: 10.1038/nprot.2007.202. View

3.
Dejardin J, Rappailles A, Cuvier O, Grimaud C, Decoville M, Locker D . Recruitment of Drosophila Polycomb group proteins to chromatin by DSP1. Nature. 2005; 434(7032):533-8. DOI: 10.1038/nature03386. View

4.
Kriegstein A, Alvarez-Buylla A . The glial nature of embryonic and adult neural stem cells. Annu Rev Neurosci. 2009; 32:149-84. PMC: 3086722. DOI: 10.1146/annurev.neuro.051508.135600. View

5.
Jobe E, McQuate A, Zhao X . Crosstalk among Epigenetic Pathways Regulates Neurogenesis. Front Neurosci. 2012; 6:59. PMC: 3347638. DOI: 10.3389/fnins.2012.00059. View