ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA757711 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15609432_1.fastq.gz | Fastqsanger.gz | |||
| SRR15609432_2.fastq.gz | Fastqsanger.gz | |||
| SRR15609433_1.fastq.gz | Fastqsanger.gz | |||
| SRR15609433_2.fastq.gz | Fastqsanger.gz | |||
| SRR15609434_1.fastq.gz | Fastqsanger.gz |
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Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global effects of MORC3 on DNA accessibility, we deleted MORC3 in IFNAR1-/- IFNAR2-/- BLaER1 monocytes and performed ATAC-seq.
2021-11-01 | GSE182752 | GEO
Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global transcriptional effects of loss of MORC3, we deleted MORC3 in WT, IFNAR1–/– IFNAR2–/– and IFNB1–/– BLaER1 monocytes and performed RNA-seq.
2021-11-01 | GSE182755 | GEO
Project description:Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]
| PRJNA757713 | ENA
Project description:We have identified a MORC3-regulated DNA element (MRE) that regulates the activation of IFNB1 upon loss of MORC3. To study the global transcriptional effects of the MRE, we deleted the MRE in STAT1–/– STAT2–/– and STAT1–/– STAT2–/– MORC3–/– BLaER1 monocytes and performed RNA-seq.
2021-11-01 | GSE182753 | GEO
Project description:We have identified that the viral virulence factors ICP0 from HSV-1 and E4ORF3 from Adenovirus5 can activate the MORC3 pathway of innate immune sensing. To study the global transcriptional effects of virulence factor sensing, we overexpressed mCherry or these virulence factors from a doxycycline-inducible lentiviral construct in BLaER1 monocytes of various genotypes and performed RNA-seq.
2021-11-01 | GSE182754 | GEO
Project description:Background: MORC proteins are involved in epigenetic gene silencing in a wide variety of eukaryotic organisms. Deletion of MORCs result in several developmental abnormalities and their dysregulation has been implicated in developmental disease and multiple cancers. Specifically, mutations of mammalian MORC3 have been associated with immune system defects, Down syndrome and human cancers such as bladder, uterine, stomach, and lung cancers, and diffuse large B cell lymphomas. While previous studies have shown that MORC3 binds to H3K4me3 in vitro and overlaps with H3K4me3 ChIP-seq peaks in mouse embryonic stem cells, the mechanism by which MORC3 regulates gene expression is unknown. Results: In this study, we find that MORC3 functions as an epigenetic silencer of endogenous retroviruses (ERVs) in mouse embryonic stem cells (mESCs). Loss of MORC3 results in upregulation of ERVs, specifically those belonging to the LTR class of retrotransposons. Using ChIP-seq, we measure the genome-wide localization of MORC3 in wild-type cells and find that MORC3 binds to ERVs suggesting its direct role in regulating ERV expression. Previous studies have shown that these ERVs are marked by repressive histone mark H3K9me3 which plays a key role in their silencing. Interestingly, we find that the levels of H3K9me3 do not change substantially upon the loss of MORC3 indicating that MORC3 possibly acts downstream of the TRIM28/SETDB1 complex that deposits H3K9me3 at these loci. Instead, we discover that loss of MORC3 results in increased chromatin accessibility at the ERVs suggesting that MORC3 silences ERVs by compacting DNA in mESCs. Conclusions: Our results reveal MORC3 as a novel regulator of ERV silencing in mouse embryonic stem cells. As early mammalian development is characterized by dynamic changes in ERV expression, the role of MORC3 in silencing ERVs is exciting and could potentially explain the abnormalities observed due to its misregulation during mammalian development.
2021-10-28 | GSE173915 | GEO
Project description:Background: MORC proteins are involved in epigenetic gene silencing in a wide variety of eukaryotic organisms. Deletion of MORCs result in several developmental abnormalities and their dysregulation has been implicated in developmental disease and multiple cancers. Specifically, mutations of mammalian MORC3 have been associated with immune system defects, Down syndrome and human cancers such as bladder, uterine, stomach, and lung cancers, and diffuse large B cell lymphomas. While previous studies have shown that MORC3 binds to H3K4me3 in vitro and overlaps with H3K4me3 ChIP-seq peaks in mouse embryonic stem cells, the mechanism by which MORC3 regulates gene expression is unknown. Results: In this study, we find that MORC3 functions as an epigenetic silencer of endogenous retroviruses (ERVs) in mouse embryonic stem cells (mESCs). Loss of MORC3 results in upregulation of ERVs, specifically those belonging to the LTR class of retrotransposons. Using ChIP-seq, we measure the genome-wide localization of MORC3 in wild-type cells and find that MORC3 binds to ERVs suggesting its direct role in regulating ERV expression. Previous studies have shown that these ERVs are marked by repressive histone mark H3K9me3 which plays a key role in their silencing. Interestingly, we find that the levels of H3K9me3 do not change substantially upon the loss of MORC3 indicating that MORC3 possibly acts downstream of the TRIM28/SETDB1 complex that deposits H3K9me3 at these loci. Instead, we discover that loss of MORC3 results in increased chromatin accessibility at the ERVs suggesting that MORC3 silences ERVs by compacting DNA in mESCs. Conclusions: Our results reveal MORC3 as a novel regulator of ERV silencing in mouse embryonic stem cells. As early mammalian development is characterized by dynamic changes in ERV expression, the role of MORC3 in silencing ERVs is exciting and could potentially explain the abnormalities observed due to its misregulation during mammalian development.
2021-10-28 | GSE173913 | GEO
Project description:Endogenous retroviruses (ERVs) comprise a significant portion of mammalian genomes. Although, specific ERV loci feature regulatory roles for host gene expression, most ERV integrations are transcriptionally repressed by Setdb1 mediated H3K9me3 and DNA methylation. However, the protein network which regulates deposition of these chromatin modifications is still incompletely understood. Here, we performed a genome-wide sgRNA screen for genes involved in ERV silencing and identified the GHKL ATPase protein Morc3 as top scoring hit. Morc3 knock-out cells display de-repression, reduced H3K9me3 and increased chromatin accessibility of distinct ERV classes. We found that the GHKL ATPase domain of Morc3 is critical for ERV silencing, since mutants which cannot bind ATP, or which are defective in ATP hydrolysis cannot rescue the Morc3 ko phenotype. Proteomic analysis revealed that Morc3 mutant protein which cannot bind ATP fails to interact with the H3.3 chaperone Daxx. This interaction depends on Morc3 sumoylation, as Daxx lacking the SUMO interaction domain shows reduced association with Morc3. Notably, in Morc3 ko cells, we observed strongly reduced H3.3 on Morc3 binding sites. Thus, our data demonstrate Morc3 as critical regulator of Daxx-mediated H3.3 incorporation into ERV regions.
2021-09-07 | GSE159932 | GEO
Project description:ATAC-seq was performed to map changes in chromatin accessibility in monocytes during in vitro differentiation. In addition to control cells, we also studied the impact of siRNA mediated knock-down of key transcription factors on accessible chromatin in monocyte-derived dendritic cells.
2021-02-03 | E-MTAB-9926 | biostudies-arrayexpress
Project description:Transcriptional profile of MRE deficient BLaER1 monocytes [RNA MRE]
| PRJNA757712 | ENA