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ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [ChIP-Seq]

ABSTRACT: ZBTB24 has emerged as a key player in DNA methylation, immunity and development. To explore these multiple facets of ZBTB24 functions, we performed and integrated multi-omics analyses in mouse and human cellular systems relevant for the physiopathological features of the ICF2 syndrome, a rare genetic disease caused by ZBTB24 mutations.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE218862 | GEO | 2025/01/30

REPOSITORIES: GEO

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ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RRBS]

Project description:ZBTB24 has emerged as a key player in DNA methylation, immunity and development. To explore these multiple facets of ZBTB24 functions, we performed and integrated multi-omics analyses in mouse and human cellular systems relevant for the physiopathological features of the ICF2 syndrome, a rare genetic disease caused by ZBTB24 mutations.

2025-01-30 | GSE218859 | GEO

ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RNA-Seq]

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Effect of Zbtb24-depletion on gene expressions during the activation of peritoneal B1 cells

Project description:ZBTB24-null ICF2 patients suffer from recurrent infections associated with antibody defects, implying a pivitol role of ZBTB24 in B cell biology. We thus generated B-cell specific Zbtb24 knockout mice and investigated its intrinsic role in B cell development and function both in vitro and in vivo. In accordance with findings obtained in ICF2 patients, Zbtb24 is dispensable for B cell developent and maintenance in mice. Strikingly, lack of Zbtb24 does not significantly compromise the primary & secondary antibody responses against TD-Ags, but reduced TID-Ags-elicited antibodies in vivo. At the cellular level, we discovered that Zbtb24-depletion specifically impaires the plasma cell (PC) differentiation of B1, but not the conventional B2 cells comprising follicular and marginal zone B cells, without impacting their survival and proliferation. Mechanistically, ablation of Zbtb24 suppresses the biosynthesis o heme in B1 cells, and supplementation of hemin largely abrogates the differentiation defects of zbtb24-null B1 cells in vitro. Our study not only provides a plausible explanation for the recurrent respiratory and gastrointestinal infections in ICF2 patients, but is also relevant for other B1 cell-mediated barrier defenses and immune regulations.

2024-09-11 | GSE241747 | GEO

Effect of Zbtb24-depletion on gene expressions during the activation of total splenic B cells

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ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats

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

2025-01-30 | GSE218867 | GEO

Loss of ZBTB24, a novel non-homologous end-joining protein, impairs class-switch recombination in ICF syndrome

Project description:The autosomal recessive immunodeficiency, centromeric instability and facial anomalies (ICF) syndrome is a genetically heterogeneous disorder. Despite recent successes in the identification of the underlying gene defects, it is currently unclear how mutations in any of the four known ICF genes cause a primary immunodeficiency. Here we demonstrate that loss of ZBTB24 in B cells from ICF2 patients impairs non-homologous end-joining (NHEJ) during immunoglobulin class-switch recombination and consequently impairs immunoglobulin production and subtype balance. Mechanistically, we found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates auto-poly(ADP-ribosyl)ation of this enzyme. The zinc finger in ZBTB24 binds PARP1-associated poly(ADP-ribose) chains and mediates the PARP1-dependent recruitment of ZBTB24 to DNA breaks. Moreover, by binding to poly(ADP-ribose) chains ZBTB24 protects these moieties from degradation by poly(ADP-ribose) glycohydrolase (PARG). This enhances the poly(ADP-ribose)-dependent interaction between PARP1 and the LIG4/XRCC4 NHEJ complex and promotes NHEJ by facilitating the assembly of this repair complex at DNA breaks. Thus, we uncover ZBTB24 as a regulator of PARP1-dependent NHEJ and class-switch recombination, providing a molecular basis for the immunodeficiency in ICF syndrome.

2020-08-19 | PXD014741 | Pride

ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats

Project description:ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats

| PRJNA906034 | ENA

ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RRBS]

Project description:ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RRBS]

| PRJNA906032 | ENA

ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RNA-Seq]

Project description:ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats [RNA-Seq]

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