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BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (ChIP-seq)

ABSTRACT: BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (ChIP-seq)

PROVIDER: PRJNA1080266 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28088006.fastq.gz	Fastqsanger.gz
	SRR28088007.fastq.gz	Fastqsanger.gz
	SRR28088008.fastq.gz	Fastqsanger.gz
	SRR28088009.fastq.gz	Fastqsanger.gz
	SRR28088010.fastq.gz	Fastqsanger.gz

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BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq)

Project description:The H3K4 methyltransferase SETD1A plays an essential role in both development and cancer. However, essential components involved in SETD1A chromatin binding remain unclear. Here, we discovered that BOD1L exhibits the highest correlated co-dependency with SETD1A in human cancer cell lines. BOD1L knockout reduces leukemia cells in vitro and in vivo, and mimics the transcriptional profiles observed in SETD1A knockout cells. The loss of BOD1L immediately reduced SETD1A distribution at transcriptional start sites (TSS) and induces transcriptional elongation defect along with the increasing of RNA polymerase II at TSS, but did not cause the reduction of H3K4me3. The Shg1 domain of BOD1L has a DNA binding ability, and recruit SETD1A to chromatin through the association with SETD1A FLOS domain. In addition, the BOD1L-SETD1A complex associates with transcriptional regulators, including E2Fs. These results reveal that BOD1L mediates chromatin and SETD1A, and regulates the non-canonical function of SETD1A in transcription.

2024-06-25 | GSE258789 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (ChIP-seq)

2024-06-25 | GSE258788 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A.

Project description:BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A.

| PRJNA1080261 | ENA

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq)

Project description:BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq)

| PRJNA1080267 | ENA

The BOD1L subunit of the SETD1A complex sustains the expression of DNA damage repair genes despite restraining H3K4 trimethylation [single_end_RNAseq]

Project description:Background SETD1A is the histone 3 lysine 4 (H3K4) methyltransferase central to the mammalian version of the highly conserved eight subunit Set1 complex (Set1C) that apparently conveys H3K4 trimethylation (H3K4me3) onto all active Pol II promoters. Accordingly, the Setd1a mouse knock-out dies in early embryogenesis at the epiblast stage and mouse embryonic stem cells (ESCs) die when SETD1A is removed. Results We report that ESC death is accompanied by loss of expression of DNA repair genes and accumulating DNA damage. BOD1L and BOD1 are homologs of the yeast Set1C subunit, Shg1, and subunits of the mammalian SETD1A and B complexes. We show that the Shg1 homology region binds to a highly conserved central a-helix in SETD1A and B. Like mutagenesis of Shg1 in yeast, conditional mutagenesis of Bod1l in ESCs promoted increased H3K4 di- and tri-methylation but also, like loss of SETD1A, loss of expression of DNA repair genes, increased DNA damage and cell death. Conclusions In contrast to similar losses of DNA repair gene expression, the converse changes in H3K4 methylation after loss of SETD1A or BOD1L implies that H3K4 methylation is not essential for expression of the DNA repair network genes. Because BOD1L becomes highly phosphorylated after DNA damage and acts to protect damaged replication forks, the SETD1A complex, and BOD1L in particular, are key nodes for the DNA damage repair network.

2026-02-18 | GSE319677 | GEO

The BOD1L subunit of the SETD1A complex sustains the expression of DNA damage repair genes despite restraining H3K4 trimethylation [paired_end_RNAseq]

2026-02-18 | GSE319676 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A.

Project description:The H3K4 methyltransferase SETD1A plays an essential role in both development and cancer. However, essential components involved in SETD1A chromatin binding remain unclear. Here, we discovered that BOD1L exhibits the highest correlated SETD1A co-dependency in human cancer cell lines. BOD1L knockout reduces leukemia cells in vitro and in vivo, and mimics the transcriptional profiles observed in SETD1A knockout cells. The loss of BOD1L immediately reduced SETD1A distribution at transcriptional start sites (TSS), induced transcriptional elongation defect, and increased the RNA polymerase II content at TSS; however, it did not reduce H3K4me3. The Shg1 domain of BOD1L has a DNA binding ability, and a tryptophan residue (W104) in the domain recruits SETD1A to chromatin through the association with SETD1A FLOS domain. In addition, the BOD1L-SETD1A complex associates with transcriptional regulators, including E2Fs. These results reveal that BOD1L mediates chromatin and SETD1A, and regulates the non-canonical function of SETD1A in transcription.

| S-EPMC11381347 | biostudies-literature

H3K4 methylation by SETD1A/BOD1L facilitates RIF1-dependent NHEJ.

Project description:The 53BP1-RIF1-shieldin pathway maintains genome stability by suppressing nucleolytic degradation of DNA ends at double-strand breaks (DSBs). Although RIF1 interacts with damaged chromatin via phospho-53BP1 and facilitates recruitment of the shieldin complex to DSBs, it is unclear whether other regulatory cues contribute to this response. Here, we implicate methylation of histone H3 at lysine 4 by SETD1A-BOD1L in the recruitment of RIF1 to DSBs. Compromising SETD1A or BOD1L expression or deregulating H3K4 methylation allows uncontrolled resection of DNA ends, impairs end-joining of dysfunctional telomeres, and abrogates class switch recombination. Moreover, defects in RIF1 localization to DSBs are evident in patient cells bearing loss-of-function mutations in SETD1A. Loss of SETD1A-dependent RIF1 recruitment in BRCA1-deficient cells restores homologous recombination and leads to resistance to poly(ADP-ribose)polymerase inhibition, reinforcing the clinical relevance of these observations. Mechanistically, RIF1 binds directly to methylated H3K4, facilitating its recruitment to, or stabilization at, DSBs.

| S-EPMC9616806 | biostudies-literature

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A.

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

2024-06-25 | GSE258792 | GEO

Set1 H3K4 methyltransferase and Jhd2 H3K4 demethylase

Project description:Set1 H3K4 methyltransferase and Jhd2 H3K4 demethylase

| PRJNA296896 | ENA