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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247620 | GEO | 2024/06/01

REPOSITORIES: GEO

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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

Project description:Short interspersed nuclear element (SINE) B2 are a type of DNA retrotransposon that organize three-dimensional genome during development. Containing binding sites for CCCTC-binding factor (CTCF), SINE_B2 serve as domain boundary elements that control chromatin state and initiate transcription of critical developmental genes. However, it is still unclear how SINE_B2 are regulated during neurodevelopment. Our findings indicate novel mechanisms that modulate critical DNA retrotransposon activity, maintain chromosome conformation and contribute to central nervous system development.

2024-06-01 | GSE247619 | GEO

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

2024-06-01 | GSE247618 | GEO

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

2024-06-01 | GSE247617 | GEO

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

| PRJNA1039825 | ENA

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

| PRJNA1039830 | ENA

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

| PRJNA1039826 | ENA

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

| PRJNA1039829 | ENA

Regulation of DNA methylation turnover at LTR retrotransposons and imprinted loci by the histone methyltransferase Setdb1.

Project description:During mammalian development, DNA methylation patterns need to be reset in primordial germ cells (PGCs) and preimplantation embryos. However, many LTR retrotransposons and imprinted genes are impervious to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that a subset of such genomic regions are resistant to widespread erasure of DNA methylation in mouse embryonic stem cells (mESCs) lacking the de novo DNA methyltransferases (Dnmts) Dnmt3a and Dnmt3b. Intriguingly, these loci are enriched for H3K9me3 in mESCs, implicating this mark in DNA methylation homeostasis. Indeed, deletion of the H3K9 methyltransferase SET domain bifurcated 1 (Setdb1) results in reduced H3K9me3 and DNA methylation levels at specific loci, concomitant with increased 5-hydroxymethylation (5hmC) and ten-eleven translocation 1 binding. Taken together, these data reveal that Setdb1 promotes the persistence of DNA methylation in mESCs, likely reflecting one mechanism by which DNA methylation is maintained at LTR retrotransposons and imprinted genes during developmental stages when DNA methylation is reprogrammed.

| S-EPMC4020067 | biostudies-literature

The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase.

Project description:SETDB1, a histone H3 lysine 9 (H3K9) methyltransferase, is crucial in meiosis and embryo development. This study aimed to investigate whether SETDB1 was associated with spermatogonial stem cells (SSC) homeostasis. We found that knockdown of Setdb1 impaired cell proliferation, led to an increase in reactive oxygen species (ROS) level through NADPH oxidase, and Setdb1 deficiency activated ROS downstream signaling pathways, including JNK and p38 MAPK, which possibly contributed to SSC apoptosis. Melatonin scavenged ROS and rescued the phenotype of Setdb1 KD. In addition, we demonstrated that SETDB1 regulated NADPH oxidase 4 (Nox4) and E2F1. Therefore, this study uncovers the new roles of SETDB1 in mediating intracellular ROS homeostasis for the survival of SSC.

| S-EPMC7567028 | biostudies-literature

SINE retrotransposons cause epigenetic reprogramming of adjacent gene promoters.

Project description:Almost half of the human genome and as much as 40% of the mouse genome is composed of repetitive DNA sequences. The majority of these repeats are retrotransposons of the SINE and LINE families, and such repeats are generally repressed by epigenetic mechanisms. It has been proposed that these elements can act as methylation centers from which DNA methylation spreads into gene promoters in cancer. Contradictory to a methylation center function, we have found that retrotransposons are enriched near promoter CpG islands that stay methylation-free in cancer. Clearly, it is important to determine which influence, if any, these repetitive elements have on nearby gene promoters. Using an in vitro system, we confirm here that SINE B1 elements can influence the activity of downstream gene promoters, with acquisition of DNA methylation and loss of activating histone marks, thus resulting in a repressed state. SINE sequences themselves did not immediately acquire DNA methylation but were marked by H3K9me2 and H3K27me3. Moreover, our bisulfite sequencing data did not support that gain of DNA methylation in gene promoters occurred by methylation spreading from SINE B1 repeats. Genome-wide analysis of SINE repeats distribution showed that their enrichment is directly correlated with the presence of USF1, USF2, and CTCF binding, proteins with insulator function. In summary, our work supports the concept that SINE repeats interfere negatively with gene expression and that their presence near gene promoters is counter-selected, except when the promoter is protected by an insulator element.

| S-EPMC3475755 | biostudies-literature

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