Arabidopsis MORC proteins function in the efficient establishment of RNA directed DNA methylation
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ABSTRACT:
PROVIDER: PRJNA672885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12922121.fastq.gz | Fastqsanger.gz | |||
| SRR12922122.fastq.gz | Fastqsanger.gz | |||
| SRR12922124.fastq.gz | Fastqsanger.gz | |||
| SRR12922125.fastq.gz | Fastqsanger.gz | |||
| SRR12922125_1.fastq.gz | Fastqsanger.gz |
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Project description:The Microrchidia (MORC) family of ATPases are required for transposable element (TE) silencing and heterochromatin condensation in plants and animals, and C. elegans MORC-1 has been shown to topologically entrap and condense DNA. In Arabidopsis thaliana, mutation of MORCs has been shown to reactivate silent methylated genes and transposons and to decondense heterochromatic chromocenters, despite only minor changes in the maintenance of DNA methylation. Here we provide the first evidence localizing Arabidopsis MORC proteins to specific regions of chromatin and find that MORC4 and MORC7 are closely co-localized with sites of RNA directed DNA methylation (RdDM). We further show that MORC7, when tethered to DNA by an artificial zinc finger, can facilitate the establishment of RdDM. Finally, we show that MORCs are required for the efficient RdDM mediated establishment of DNA methylation and silencing of a newly integrated FWA transgene, even though morc mutations have no effect on the maintenance of preexisting methylation at the endogenous FWA gene. We propose that MORCs function as a molecular tether in RdDM complexes to reinforce RdDM activity for methylation establishment. These findings have implications for MORC protein function in a variety of other eukaryotic organisms.
2021-07-02 | GSE160285 | GEO
Project description:The Microrchidia (MORC) family of ATPases are required for transposable element (TE) silencing and heterochromatin condensation in plants and animals, and C. elegans MORC-1 has been shown to topologically entrap and condense DNA. In Arabidopsis thaliana, mutation of MORCs has been shown to reactivate silent methylated genes and transposons and to decondense heterochromatic chromocenters, despite only minor changes in the maintenance of DNA methylation. Here we provide the first evidence localizing Arabidopsis MORC proteins to specific regions of chromatin and find that MORC4 and MORC7 are closely co-localized with sites of RNA directed DNA methylation (RdDM). We further show that MORC7, when tethered to DNA by an artificial zinc finger, can facilitate the establishment of RdDM. Finally, we show that MORCs are required for the efficient RdDM mediated establishment of DNA methylation and silencing of a newly integrated FWA transgene, even though morc mutations have no effect on the maintenance of preexisting methylation at the endogenous FWA gene. We propose that MORCs function as a molecular tether in RdDM complexes to reinforce RdDM activity for methylation establishment. These findings have implications for MORC protein function in a variety of other eukaryotic organisms.
2021-07-02 | PXD026674 | Pride
Project description:The Microrchidia (MORC) family proteins are evolutionarily conserved GHKL type ATPases involved in chromatin compaction and gene silencing. Arabidopsis MORC proteins act in the RNA-directed DNA methylation (RdDM) pathway where they act as molecular tethers to ensure the efficient establishment of RdDM and de novo gene silencing. However, they also have RdDM independent functions in which the underlying mechanism is unknown. In this study, we examined MORC binding regions that are devoid of RdDM to shed light on MORCs RdDM independent functions. We found that MORC proteins can compact chromatin, exclude the accessibility of DNA to transcription factors (TFs) and thereby repress gene expression. We also found that MORC-mediated repression is particularly important under stress conditions. In addition, we showed that MORC proteins may regulate TFs through direct or indirect interactions. These TFs in turn regulate their own transcription, indicating a feedforward loop. Our findings provide insights into the molecular mechanisms of MORC-mediated chromatin compaction and transcription regulation.
2023-03-27 | GSE212801 | GEO
Project description:The Microrchidia (MORC) family of ATPases are required for transposable element (TE) silencing and heterochromatin condensation in plants and animals, and C. elegans MORC-1 has been shown to topologically entrap and condense DNA. In Arabidopsis thaliana, mutation of MORCs has been shown to reactivate silent methylated genes and transposons and to decondense heterochromatic chromocenters, despite only minor changes in the maintenance of DNA methylation. Here we provide the first evidence localizing Arabidopsis MORC proteins to specific regions of chromatin and find that MORC4 and MORC7 are closely co-localized with sites of RNA-directed DNA methylation (RdDM). We further show that MORC7, when tethered to DNA by an artificial zinc finger, can facilitate the establishment of RdDM. Finally, we show that MORCs are required for the efficient RdDM mediated establishment of DNA methylation and silencing of a newly integrated FWA transgene, even though morc mutations have no effect on the maintenance of preexisting methylation at the endogenous FWA gene. We propose that MORCs function as a molecular tether in RdDM complexes to reinforce RdDM activity for methylation establishment. These findings have implications for MORC protein function in a variety of other eukaryotic organisms.
| S-EPMC8277788 | biostudies-literature
Project description:Transposable elements (TEs) and DNA repeats are commonly targeted by DNA and histone methylation to achieve epigenetic gene silencing. We isolated mutations in two Arabidopsis genes, CRT1 and CRH6, which cause de-repression of DNA-methylated genes and TEs, but no losses of DNA or histone methylation. CRT1 and CRH6 are members of the conserved Microrchidia (MORC) ATPase family, predicted to catalyze alterations in chromosome superstructure. The crt1 and crh6 mutants show decondensation of pericentromeric heterochromatin, increased interaction of pericentromeric regions with the rest of the genome, and transcriptional defects that are largely restricted to loci residing in pericentromeric regions. Knockdown of the single MORC homolog in Caenorhabditis elegans also impairs transgene silencing. We propose that the MORC ATPases are conserved regulators of gene silencing in eukaryotes. For Col wild type control and each of two T-DNA mutants, a single sample each of small RNA (sRNA), mRNA-Seq, 5'-methylcytosine DNA methylation (BS-Seq), ChIP H3K9me2 histone methylation, and ChIP H3 histone control. For each of two EMS mutants, and as controls, their respective backgrounds, two batches of single mRNA samples, with the first batch also having a single mRNA sample for a double EMS mutant.
2012-05-02 | E-GEOD-37644 | biostudies-arrayexpress
Project description:The germline is an immortal cell lineage and therefore must accurately transmit genetic and epigenetic information over infinite cell divisions to ensure fertility and species survival. Endogenous siRNAs (endo-siRNAs), which are highly expressed in the parental germline and inherited in their progeny, represent one mechanism by which epigenetic information can be transmitted from one generation to the next. In C. elegans, this is accomplished by the nuclear RNAi pathway, which ensures robust inheritance of endo-siRNAs and of target gene silencing through deposition of H3K9me3 marks at target loci. How these marks are maintained in subsequent generations is unknown. Here, we show that the C. elegans micro-orchidia homolog, MORC-1, functions downstream of endo-siRNAs to mediate target silencing and maintenance of siRNA-dependent H3K9me3 marks. Like the established members of the nuclear RNAi pathway, morc-1 is essential for germline maintenance and thus morc-1(-) mutants exhibit a mortal germline phenotype. Furthermore, morc-1(-) mutants exhibit severe decondensation of germline chromatin. Through a forward genetic screen, we have identified mutations in the gene encoding MET-1, a H3K36 histone methyltransferase, that potently suppress morc-1(-) germline mortality. We show that morc-1(-) mutants exhibit progressive, met-1-dependent enrichment of H3K36me3 and that mutation of met-1 can restore germline chromatin organization in late generation morc-1(-) mutants. Our data suggest that MORC-1 is required to repress MET-1 activity at nuclear RNAi target genes and that in the absence of this repression, MET-1-mediated encroachment of euchromatin leads to detrimental decondensation of germline chromatin and germline mortality.
2017-05-22 | GSE89887 | GEO
Project description:The MORC (microrchidia) family of proteins is highly conserved in all eukaryotic cells and have been shown to play diverse roles by forming protein-protein interactions with immune-responsive proteins, SWI chromatin remodeling complexes, histone deacetylases, and histone tail modifications across metazoans. To dissect the functional roles of MORC in the human malaria parasite, Plasmodium falciparum, we developed a glmS based ribozyme knockdown system to induce PfMORC knockdown upon glucosamine (GlcN) induction. We further conducted a transcriptomic analysis in PfMORC-HA-glmS knockdown parasites at the asexual stage to investigate alterations in global gene expression. Our results indicate an overrepresentation of downregulated genes belonging to the heterochromatin-associated hypervariable gene family proteins. Overall, we found that PfMORC controls the asexual gene expression of the P. falciparum and can be a potential target for malaria disease containment.
2023-11-15 | GSE241313 | GEO
Project description:MORC proteins regulate transcription factor binding through mediating chromatin compaction at active chromatin regions
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Project description:HiChIP: Efficient and sensitive analysis of protein-directed genome architecture
| PRJNA320090 | ENA
Project description:Transposable elements (TEs) and DNA repeats are commonly targeted by DNA and histone methylation to achieve epigenetic gene silencing. We isolated mutations in two Arabidopsis genes, CRT1 and CRH6, which cause de-repression of DNA-methylated genes and TEs, but no losses of DNA or histone methylation. CRT1 and CRH6 are members of the conserved Microrchidia (MORC) ATPase family, predicted to catalyze alterations in chromosome superstructure. The crt1 and crh6 mutants show decondensation of pericentromeric heterochromatin, increased interaction of pericentromeric regions with the rest of the genome, and transcriptional defects that are largely restricted to loci residing in pericentromeric regions. Knockdown of the single MORC homolog in Caenorhabditis elegans also impairs transgene silencing. We propose that the MORC ATPases are conserved regulators of gene silencing in eukaryotes.
2012-05-03 | GSE37644 | GEO