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Tytuł pozycji:

Identification of aberrant transcription termination at specific gene loci with DNA hypomethylated transcription termination sites caused by DNA methyltransferase deficiency.

Tytuł:
Identification of aberrant transcription termination at specific gene loci with DNA hypomethylated transcription termination sites caused by DNA methyltransferase deficiency.
Autorzy:
Shirai M; Department of Biological Science, Graduate School of Science, Hiroshima University.
Nara T; Graduate School of Integrated Sciences for Life, Hiroshima University.
Takahashi H; Department of Biological Science, Graduate School of Science, Hiroshima University.; Graduate School of Integrated Sciences for Life, Hiroshima University.
Takayama K; Department of Biological Science, Graduate School of Science, Hiroshima University.
Chen Y; Graduate School of Integrated Sciences for Life, Hiroshima University.
Hirose Y; Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University.
Fujii M; Graduate School of Integrated Sciences for Life, Hiroshima University.
Awazu A; Graduate School of Integrated Sciences for Life, Hiroshima University.
Shimoda N; Laboratory of Molecular Analysis, Research and Development Management Center, National Center for Geriatrics and Gerontology.
Kikuchi Y; Department of Biological Science, Graduate School of Science, Hiroshima University.; Graduate School of Integrated Sciences for Life, Hiroshima University.
Źródło:
Genes & genetic systems [Genes Genet Syst] 2022 Oct 18; Vol. 97 (3), pp. 139-152. Date of Electronic Publication: 2022 Sep 06.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Mishima, Shizuoka, Japan : Genetics Society of Japan, 1996-
MeSH Terms:
DNA (Cytosine-5-)-Methyltransferases*/genetics
DNA (Cytosine-5-)-Methyltransferases*/metabolism
DNA Methylation*
Mice ; Animals ; Promoter Regions, Genetic ; DNA ; Transcription, Genetic ; Epigenomics ; DNA Methyltransferase 3A
Contributed Indexing:
Keywords: DNA methylation; Dnmt3a; chimeric transcript; read-through transcript; transcription termination
Substance Nomenclature:
EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases)
9007-49-2 (DNA)
EC 2.1.1.37 (DNA Methyltransferase 3A)
Entry Date(s):
Date Created: 20220619 Date Completed: 20221021 Latest Revision: 20221021
Update Code:
20240105
DOI:
10.1266/ggs.21-00092
PMID:
35718462
Czasopismo naukowe
CpG methylation of genomic DNA is a well-known repressive epigenetic marker in eukaryotic transcription, and DNA methylation of promoter regions is correlated with gene silencing. In contrast to the promoter regions, the function of DNA methylation during transcription termination remains to be elucidated. A recent study revealed that mouse DNA methyltransferase 3a (Dnmt3a) mainly functions in de novo methylation in the promoter and gene body regions, including transcription termination sites (TTSs), during development. To investigate the relationship between DNA methylation overlapping the TTSs and transcription termination, we performed bioinformatics analysis using six pre-existing Dnmt -/- mouse cell datasets: four types of neurons (three Dnmt3a -/- and one Dnmt1 -/- mutants) and two types of embryonic fibroblasts (MEFs) (Dnmt3a -/- and Dnmt3b -/- mutants). Combined analyses using methylome and transcriptome data revealed that read counts downstream of hypomethylated TTSs were increased in three types of neurons (two Dnmt3a -/- and one Dnmt1 -/- mutants). Among these, an increase in chimeric transcripts downstream of the TTSs was observed in Dnmt3a -/- mature olfactory sensory neurons and Dnmt3a -/- agouti-related peptide (protein)-producing neurons, thereby indicating that read-through occurs in hypomethylated TTSs at specific gene loci in these two mutants. Conversely, in Dnmt3a -/- MEFs, we detected reductions in read counts downstream of hypomethylated TTSs. These results indicate that the hypomethylation of TTSs can both positively and negatively regulate transcription termination, dependent on Dnmt and cell types. This study is the first to identify the aberrant termination of transcription at specific gene loci with DNA hypomethylated TTSs attributable to Dnmt deficiency.

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