Folate Carrier Deficiency Drives Differential Methylation and Enhanced Cellular Potency in the Neural Plate Border.
DNA methylation
NOTCH1
folate
neural plate
neural plate border
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
13
12
2021
accepted:
07
06
2022
entrez:
1
8
2022
pubmed:
2
8
2022
medline:
2
8
2022
Statut:
epublish
Résumé
The neural plate border (NPB) of vertebrate embryos segregates from the neural and epidermal regions, and it is comprised of an intermingled group of multipotent progenitor cells. Folate is the precursor of S-adenosylmethionine, the main methyl donor for DNA methylation, and it is critical for embryonic development, including the specification of progenitors which reside in the NPB. Despite the fact that several intersecting signals involved in the specification and territorial restriction of NPB cells are known, the role of epigenetics, particularly DNA methylation, has been a matter of debate. Here, we examined the temporal and spatial distribution of the methyl source and analyzed the abundance of 5mC/5 hmC and their epigenetic writers throughout the segregation of the neural and NPB territories. Reduced representation bisulfite sequencing (RRBS) on Reduced Folate Carrier 1 (RFC1)-deficient embryos leads to the identification of differentially methylated regions (DMRs). In the RFC1-deficient embryos, we identified several DMRs in the
Identifiants
pubmed: 35912103
doi: 10.3389/fcell.2022.834625
pii: 834625
pmc: PMC9326018
doi:
Types de publication
Journal Article
Langues
eng
Pagination
834625Informations de copyright
Copyright © 2022 Alata Jimenez and Strobl-Mazzulla.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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