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Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome

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

ORGANISM(S): Mus musculus

PROVIDER: GSE200729 | GEO | 2022/04/14

REPOSITORIES: GEO

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Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome (MIRA-seq)

Project description:Mutagenic purine-pyrimidine repeats can adopt the left-handed Z-DNA conformation. DNA breaks at potential Z-DNA sites can lead to somatic mutations in cancer or to germ line mutations which are transmitted to the next generation. It is not known whether any mechanism exists in the germ line to control Z-DNA structure and DNA breaks at purine-pyrimidine repeats. Here, we provide genetic, epigenomic, and biochemical evidence for the existence of a biological process that erases Z-DNA specifically in germ cells of the mouse male fetus. We show that a previously uncharacterized zinc finger protein, ZBTB43, binds to and removes Z-DNA, preventing the formation of DNA double-strand breaks. By removing Z-DNA, ZBTB43 also promotes de novo DNA methylation at CG-containing purine-pyrimidine repeats in prospermatogonia. Therefore, the genomic and epigenomic integrity of the species is safeguarded by remodeling DNA structure in the mammalian germ line during a critical window of germline epigenome reprogramming.

2022-04-14 | GSE200728 | GEO

Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome (ChIP-seq)

2022-04-14 | GSE200722 | GEO

Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome (Affinity-seq)

2022-04-14 | GSE200719 | GEO

Z-DNA is remodelled by ZBTB43 in prospermatogonia to safeguard the germline genome and epigenome.

Project description:Mutagenic purine-pyrimidine repeats can adopt the left-handed Z-DNA conformation. DNA breaks at potential Z-DNA sites can lead to somatic mutations in cancer or to germline mutations that are transmitted to the next generation. It is not known whether any mechanism exists in the germ line to control Z-DNA structure and DNA breaks at purine-pyrimidine repeats. Here we provide genetic, epigenomic and biochemical evidence for the existence of a biological process that erases Z-DNA specifically in germ cells of the mouse male foetus. We show that a previously uncharacterized zinc finger protein, ZBTB43, binds to and removes Z-DNA, preventing the formation of DNA double-strand breaks. By removing Z-DNA, ZBTB43 also promotes de novo DNA methylation at CG-containing purine-pyrimidine repeats in prospermatogonia. Therefore, the genomic and epigenomic integrity of the species is safeguarded by remodelling DNA structure in the mammalian germ line during a critical window of germline epigenome reprogramming.

| S-EPMC9276527 | biostudies-literature

Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome

Project description:Z-DNA is Remodeled by ZBTB43 in Prospermatogonia to Safeguard the Germ Line Genome and Epigenome

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Safeguard function of PU.1 shapes the inflammatory epigenome of neutrophils

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-19 | GSE110865 | GEO

Gene expression in germ line

Project description:Identification of genes expressed in the germ line of C. elegans. This SuperSeries is composed of the SubSeries listed below.

2003-12-24 | GSE696 | GEO

Genome-wide methylation profiles in primary intracranial germ cell tumors indicate primordial germ cell origin of germinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Genome-wide investigation of the dynamic changes of epigenome modifications after DNA methylation editing

Project description:This SuperSeries is composed of the SubSeries listed below.

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Hypersensitivity to DNA damage in antephase as a safeguard for genome stability.

Project description:Activation of the DNA-damage response can lead to the induction of an arrest at various stages in the cell cycle. These arrests are reversible in nature, unless the damage is too excessive. Here we find that checkpoint reversibility is lost in cells that are in very late G2, but not yet fully committed to enter mitosis (antephase). We show that antephase cells exit the cell cycle and enter senescence at levels of DNA damage that induce a reversible arrest in early G2. We show that checkpoint reversibility critically depends on the presence of the APC/C inhibitor Emi1, which is degraded just before mitosis. Importantly, ablation of the cell cycle withdrawal mechanism in antephase promotes cell division in the presence of broken chromosomes. Thus, our data uncover a novel, but irreversible, DNA-damage response in antephase that is required to prevent the propagation of DNA damage during cell division.

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