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Ena-DATASET-DCPTCUHK-02-10-2019-08:22:44:584-170 - samples

ABSTRACT: The biology of cell-free DNA fragmentation and the roles of DNASE1, DNASE1L3 and DFFB

PROVIDER: EGAD00001005371 | EGA |

REPOSITORIES: EGA

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The biology of cell-free DNA fragmentation and the roles ofDNASE1, DNASE1L3 and DFFB

Project description:The biology of cell-free DNA fragmentation and the roles of DNASE1, DNASE1L3 and DFFB

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Nuclease deficiencies alter plasma cell-free DNA methylationprofiles (mouse)

Project description:The effects of DNASE1L3 or DNASE1 deficiency on cfDNA methylation was explored in plasma of mice deficient in these nucleases and in DNASE1L3-deficient humans. Compared to wildtype cfDNA, cfDNA in Dnase1l3-deficient mice was significantly hypomethylated, while cfDNA in Dnase1-deficient mice was hypermethylated. The cfDNA hypomethylation in Dnase1l3-deficient mice was due to increased fragmentation and representation from open chromatin regions (OCRs) and CpG islands (CGIs). These findings were absent in Dnase1-deficient mice.

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Project description:We showed that mice in which Dnase1l3 had been deleted showed aberrations in the fragmentation of plasma DNA. We also observed a change in the ranked frequencies of end motifs of plasma DNA caused by the Dnase1l3 deletion.

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ena-DATASET-DCPTCUHK-07-06-2021-04:58:11:091-720 - samples

Project description:The dataset contains sequencing data in wildtype, Dnase1-deficient and Dnase1l3-deficient mice. We performed 2 x 75bp paired-end whole genome bisulfite sequencing of pooled plasma cell-free DNA (cfDNA) and buffy coat genomic DNA. The effects of DNASE1L3 or DNASE1 deficiency on cfDNA methylation was explored in plasma of mice deficient in these nucleases.

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Dnase1l3 knockout causes aberrations in plasma DNA fragmentation

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B-cell-intrinsic DNase1L3 is essential for T-cell-independent type II response in mice

Project description:T-cell independent type II (TI-II) antigens, such as capsular polysaccharides, have multivalent epitope, which induce B cell activation, plasma cell differentiation and antibody production by strongly cross-linking B cell receptors. However, the mechanism of B cell activation by TI-II antigens remains unclear. In this study, we demonstrate that DNA endonuclease DNase1L3 (also termed DNase g) is required for the TI-II response. The production of antigen-specific antibodies was severely diminished in DNase1L3-deficient mice upon immunization with TI-II antigens, but not with TD antigens. Bone-marrow chimeric mice and B cell transfer experiments revealed that B-cell-intrinsic DNase1L3 was required for the TI-II response. DNase1L3-deficient B cells were defective in cell proliferation and plasma cell differentiation in the TI-II response in vivo as well as in vitro, which was not rescued by co-culture with DNase1L3-sufficient B cells in vitro, disproving an involvement of a secretory DNase1L3. In vitro stimulation with TI-II antigen transiently increased expression of DNase1L3 and its translocation into the nucleus. RNA-seq analysis of ex-vivo B cells having been responded to TI-II antigen in vivo revealed a marked reduction of Myc-target gene sets in DNase1L3-deficient B cells. Expression of IRF4, the gene of which is a target of Myc, was diminished in the ex-vivo DNase1L3-deficient B cells, in which forced expression of IRF4 restored the TI-II response in vivo. These data revealed an unexpected role of DNase1L3 in a missing link between B cell receptor signaling and B cell activation in the TI-II response, giving a valuable clue to molecularly dissect this response.

2023-12-18 | GSE221036 | GEO

ena-DATASET-DCPTCUHK-12-06-2020-14:07:24:130-345 - samples

Project description:Human dnase1l3 deficiency-Mouse AAV samples

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Project description:Plasma DNA profile in DNASE1L3 deficiency

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