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Stricker, S.H. ; Götz, M.

DNA-methylation: Master or slave of neural fate decisions?

Front. Neurosci. 12:5 (2018)
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Open Access Gold
Creative Commons Lizenzvertrag
The pristine formation of complex organs depends on sharp temporal and spatial control of gene expression. Therefore, epigenetic mechanisms have been frequently attributed a central role in controlling cell fate determination. A prime example for this is the first discovered and still most studied epigenetic mark, DNA methylation, and the development of the most complex mammalian organ, the brain. Recently, the field of epigenetics has advanced significantly: new DNA modifications were discovered, epigenomic profiling became widely accessible, and methods for targeted epigenomic manipulation have been developed. Thus, it is time to challenge established models of epigenetic gene regulation. Here, we review the current state of knowledge about DNA modifications, their epigenomic distribution, and their regulatory role. We will summarize the evidence suggesting they possess crucial roles in neurogenesis and discuss whether this likely includes lineage choice regulation or rather effects on differentiation. Finally, we will attempt an outlook on how questions, which remain unresolved, could be answered soon.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Dna Methylation ; Dna Modification ; Epigenetics ; Epigenomics ; Neurogenesis; De-novo Methylation; Gene-expression; Endogenous Retroviruses; Methyltransferase Gene; Cytosine Methylation; Nervous-system; Cpg Island; Stem-cells; Deoxyribonucleic-acid; Postnatal-development
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 1662-453X
Zeitschrift Frontiers in Neuroscience
Quellenangaben Band: 12, Heft: , Seiten: , Artikelnummer: 5 Supplement: ,
Verlag Frontiers
Verlagsort Lausanne
Institut(e) Institute of Stem Cell Research (ISF)
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Stem Cell and Neuroscience
PSP-Element(e) G-500800-001
DOI 10.3389/fnins.2018.00005
WOS ID WOS:000423822300001
Scopus ID 85041859370
Erfassungsdatum 2018-06-04
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