Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease
Neurogenesis is an elegantly coordinated developmental process that must maintain a careful balance of proliferation and differentiation programs to be compatible with life. Due to the fine-tuning required for these processes, epigenetic mechanisms (e.g., DNA methylation and histone modifications) a...
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| Format: | Article |
| Language: | English |
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MDPI AG
2019-03-01
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| Series: | Biology |
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| Online Access: | http://www.mdpi.com/2079-7737/8/1/11 |
| _version_ | 1797728629691514880 |
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| author | Rochelle N. Wickramasekara Holly A. F. Stessman |
| author_facet | Rochelle N. Wickramasekara Holly A. F. Stessman |
| author_sort | Rochelle N. Wickramasekara |
| collection | DOAJ |
| description | Neurogenesis is an elegantly coordinated developmental process that must maintain a careful balance of proliferation and differentiation programs to be compatible with life. Due to the fine-tuning required for these processes, epigenetic mechanisms (e.g., DNA methylation and histone modifications) are employed, in addition to changes in mRNA transcription, to regulate gene expression. The purpose of this review is to highlight what we currently know about histone 4 lysine 20 (H4K20) methylation and its role in the developing brain. Utilizing publicly-available RNA-Sequencing data and published literature, we highlight the versatility of H4K20 methyl modifications in mediating diverse cellular events from gene silencing/chromatin compaction to DNA double-stranded break repair. From large-scale human DNA sequencing studies, we further propose that the lysine methyltransferase gene, KMT5B (OMIM: 610881), may fit into a category of epigenetic modifier genes that are critical for typical neurodevelopment, such as EHMT1 and ARID1B, which are associated with Kleefstra syndrome (OMIM: 610253) and Coffin-Siris syndrome (OMIM: 135900), respectively. Based on our current knowledge of the H4K20 methyl modification, we discuss emerging themes and interesting questions on how this histone modification, and particularly KMT5B expression, might impact neurodevelopment along with current challenges and potential avenues for future research. |
| first_indexed | 2024-03-12T11:16:52Z |
| format | Article |
| id | doaj.art-8c3132a6312949a8bdb795b71d6c6af8 |
| institution | Directory Open Access Journal |
| issn | 2079-7737 |
| language | English |
| last_indexed | 2024-03-12T11:16:52Z |
| publishDate | 2019-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biology |
| spelling | doaj.art-8c3132a6312949a8bdb795b71d6c6af82023-09-02T01:51:03ZengMDPI AGBiology2079-77372019-03-01811110.3390/biology8010011biology8010011Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental DiseaseRochelle N. Wickramasekara0Holly A. F. Stessman1Department of Pharmacology, School of Medicine, Creighton University, Omaha, NE 68178, USADepartment of Pharmacology, School of Medicine, Creighton University, Omaha, NE 68178, USANeurogenesis is an elegantly coordinated developmental process that must maintain a careful balance of proliferation and differentiation programs to be compatible with life. Due to the fine-tuning required for these processes, epigenetic mechanisms (e.g., DNA methylation and histone modifications) are employed, in addition to changes in mRNA transcription, to regulate gene expression. The purpose of this review is to highlight what we currently know about histone 4 lysine 20 (H4K20) methylation and its role in the developing brain. Utilizing publicly-available RNA-Sequencing data and published literature, we highlight the versatility of H4K20 methyl modifications in mediating diverse cellular events from gene silencing/chromatin compaction to DNA double-stranded break repair. From large-scale human DNA sequencing studies, we further propose that the lysine methyltransferase gene, KMT5B (OMIM: 610881), may fit into a category of epigenetic modifier genes that are critical for typical neurodevelopment, such as EHMT1 and ARID1B, which are associated with Kleefstra syndrome (OMIM: 610253) and Coffin-Siris syndrome (OMIM: 135900), respectively. Based on our current knowledge of the H4K20 methyl modification, we discuss emerging themes and interesting questions on how this histone modification, and particularly KMT5B expression, might impact neurodevelopment along with current challenges and potential avenues for future research.http://www.mdpi.com/2079-7737/8/1/11H4K20KMT5AKMT5BKMT5CSUV420Hlysine-methylationneurodevelopmentmutationsepigenetichistone methylation |
| spellingShingle | Rochelle N. Wickramasekara Holly A. F. Stessman Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease Biology H4K20 KMT5A KMT5B KMT5C SUV420H lysine-methylation neurodevelopment mutations epigenetic histone methylation |
| title | Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease |
| title_full | Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease |
| title_fullStr | Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease |
| title_full_unstemmed | Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease |
| title_short | Histone 4 Lysine 20 Methylation: A Case for Neurodevelopmental Disease |
| title_sort | histone 4 lysine 20 methylation a case for neurodevelopmental disease |
| topic | H4K20 KMT5A KMT5B KMT5C SUV420H lysine-methylation neurodevelopment mutations epigenetic histone methylation |
| url | http://www.mdpi.com/2079-7737/8/1/11 |
| work_keys_str_mv | AT rochellenwickramasekara histone4lysine20methylationacaseforneurodevelopmentaldisease AT hollyafstessman histone4lysine20methylationacaseforneurodevelopmentaldisease |