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The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases

Epigenetic mechanisms, including DNA and histone modifications, are pivotal for normal brain development and functions by modulating spatial and temporal gene expression. Dysregulation of the epigenetic machinery can serve as a causal role in numerous brain disorders. Proper mammalian brain developm...

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Autores principales: Kuehner, Janise N., Yao, Bing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8078026/
https://www.ncbi.nlm.nih.gov/pubmed/33912356
http://dx.doi.org/10.3390/epigenomes3030017
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author Kuehner, Janise N.
Yao, Bing
author_facet Kuehner, Janise N.
Yao, Bing
author_sort Kuehner, Janise N.
collection PubMed
description Epigenetic mechanisms, including DNA and histone modifications, are pivotal for normal brain development and functions by modulating spatial and temporal gene expression. Dysregulation of the epigenetic machinery can serve as a causal role in numerous brain disorders. Proper mammalian brain development and functions depend on the precise expression of neuronal-specific genes, transcription factors and epigenetic modifications. Antagonistic polycomb and trithorax proteins form multimeric complexes and play important roles in these processes by epigenetically controlling gene repression or activation through various molecular mechanisms. Aberrant expression or disruption of either protein group can contribute to neurodegenerative diseases. This review focus on the current progress of Polycomb and Trithorax complexes in brain development and disease, and provides a future outlook of the field.
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spelling pubmed-80780262021-04-27 The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases Kuehner, Janise N. Yao, Bing Epigenomes Review Epigenetic mechanisms, including DNA and histone modifications, are pivotal for normal brain development and functions by modulating spatial and temporal gene expression. Dysregulation of the epigenetic machinery can serve as a causal role in numerous brain disorders. Proper mammalian brain development and functions depend on the precise expression of neuronal-specific genes, transcription factors and epigenetic modifications. Antagonistic polycomb and trithorax proteins form multimeric complexes and play important roles in these processes by epigenetically controlling gene repression or activation through various molecular mechanisms. Aberrant expression or disruption of either protein group can contribute to neurodegenerative diseases. This review focus on the current progress of Polycomb and Trithorax complexes in brain development and disease, and provides a future outlook of the field. MDPI 2019-08-21 /pmc/articles/PMC8078026/ /pubmed/33912356 http://dx.doi.org/10.3390/epigenomes3030017 Text en © 2019 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Kuehner, Janise N.
Yao, Bing
The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title_full The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title_fullStr The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title_full_unstemmed The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title_short The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases
title_sort dynamic partnership of polycomb and trithorax in brain development and diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8078026/
https://www.ncbi.nlm.nih.gov/pubmed/33912356
http://dx.doi.org/10.3390/epigenomes3030017
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