Neurogenic to Gliogenic Fate Transition Perturbed by Loss of HMGB2

Bronstein, R., Kyle, J., Abraham, A. B., Tsirka, S. E. (2017) Neurogenic to Gliogenic Fate Transition Perturbed by Loss of HMGB2. Front Mol Neurosci, 10. p. 153. ISSN 1662-5099

URL: https://www.ncbi.nlm.nih.gov/pubmed/28588451
DOI: 10.3389/fnmol.2017.00153

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.

Item Type: Paper
Uncontrolled Keywords: Hmgb2 chromatin epigenetics histone modification postnatal neurogenesis
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > Chromatin dynamics
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > epigenetics
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > epigenetics

bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > histone
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > neurogenesis
CSHL Authors:
Communities: CSHL labs > Tollkuhn lab
Depositing User: Matt Covey
Date Deposited: 09 Jun 2017 13:16
Last Modified: 09 Jun 2017 13:16
PMCID: PMC5440561
Related URLs:
URI: http://repository.cshl.edu/id/eprint/34925

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