Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA757713 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15609718_1.fastq.gz | Fastqsanger.gz | |||
| SRR15609718_2.fastq.gz | Fastqsanger.gz | |||
| SRR15609719_1.fastq.gz | Fastqsanger.gz | |||
| SRR15609719_2.fastq.gz | Fastqsanger.gz | |||
| SRR15609720_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 transcriptional effects of loss of MORC3, we deleted MORC3 in WT, IFNAR1–/– IFNAR2–/– and IFNB1–/– BLaER1 monocytes and performed RNA-seq.
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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.
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Project description:ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]
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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.
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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.
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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 the 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 a top-scoring hit. Morc3 knock-out cells display de-repression, reduced H3K9me3, and increased chromatin accessibility of distinct ERV families. We found that the Morc3 ATPase cycle and Morc3 SUMOylation are important for ERV chromatin regulation. Proteomic analysis revealed that Morc3 mutant proteins fail to interact with the histone H3.3 chaperone Daxx. This interaction depends on Morc3 SUMOylation and Daxx SUMO binding. Notably, in Morc3 ko cells, we observed strongly reduced histone H3.3 on Morc3 binding sites. Thus, our data demonstrate Morc3 as a critical regulator of Daxx-mediated histone H3.3 incorporation to ERV regions. This dataset comprises several experiments addressing different questions: 1. ChIP-MS experiment to determine the protein interaction context of Morc3 using a Morc3-3xFLAG knock-in ES cell line compared to wild type ES cells (Experiment 20200408). 2. ChIP-MS experiments to investigate changes in the protein interaction context of the Morc3 mutant rescue cell lines. Comparison of Morc3 knock-out cell lines with re-expression of Morc3-CW-3xFLAG mutant (Ref. #3111), Morc3-ATP-binding-3xFLAG and Morc3-SUMOylation-3xFLAG mutants (Ref. #3635), and Morc3-deltaN-3xFLAG mutant (Ref. #5174) compared to wt Morc3-3XFLAG rescue. 3. ChIP-MS experiment to determine if the interaction between Morc3 and Daxx is mediated through this C-terminal SIM, comparing Daxx knock-out cell lines with re-expression of wild type 3xFLAG-Daxx protein or 3xFLAG-Daxx ∆SIM, which lacks the C-terminal SIM domain. (Ref. #3301)
2021-11-03 | PXD027368 | Pride
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 | GSE159933 | 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 | GSE159935 | GEO