The MOM1 complex recruits the RdDM machinery via MORC6 to establish de novo DNA methylation.
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE221679 | GEO | 2023/06/09
REPOSITORIES: GEO
Similar Datasets
Project description:MOM1 is an Arabidopsis factor previously shown to mediate transcriptional silencing independent of major DNA methylation changes. Here we found that MOM1 localizes with sites of RNA-directed DNA methylation (RdDM). Tethering MOM1 with artificial zinc finger to unmethylated FWA promoter led to establishment of DNA methylation and FWA silencing. This process was blocked by mutations in components of the Pol V arm of the RdDM machinery, as well as by mutation of MORC6. We found that at some endogenous RdDM sites, MOM1 is required to maintain DNA methylation and a closed chromatin state. In addition, efficient silencing of newly introduced FWA transgenes was impaired by mutation of MOM1 or mutation of genes encoding the MOM1 interacting PIAL1/2 proteins. In addition to RdDM sites, we identified a group of MOM1 peaks at active chromatin near genes that colocalized with MORC6. These findings demonstrate a multifaceted role of MOM1 in genome regulation.
2023-06-10 | PXD039991 | Pride
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 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:In plants, multiple levels of epigenetic control suppress transposon movement and permit somatic as well as transgenerational transmission of gene expression patterns. A variety of factors are involved that establish and/or maintain epigenetic marks, such as covalent modification of DNA and histones. Alteration of epigenetic marks leads to the enhancement or release of transcriptional gene silencing (TGS). TGS regulator MOM1 is special in this respect since it silences transcription by an unknown mechanism operating without obvious changes in epigenetic marks. We have isolated an enhancer of the mom1 mutation that points towards regulatory interplay between MOM1 and the plant-specific RNA Polymerase V (Pol V). Pol V transcribes heterochromatic loci and silences them. Although its biochemical properties have been studied; it is still not clear how Pol V is targeted to heterochromatin. We now provide evidence that Pol V is required for MOM1-mediated suppression of transcription at a subset of its chromosomal targets. Thus, Pol V interacts with MOM1 in the control of gene silencing. Interestingly, functional relationships between mutations in MOM1 and Pol V genes range from enhancement to independence or even suppression at different target loci.
2009-11-24 | GSE17940 | GEO
Project description:In plants, multiple levels of epigenetic control suppress transposon movement and permit somatic as well as transgenerational transmission of gene expression patterns. A variety of factors are involved that establish and/or maintain epigenetic marks, such as covalent modification of DNA and histones. Alteration of epigenetic marks leads to the enhancement or release of transcriptional gene silencing (TGS). TGS regulator MOM1 is special in this respect since it silences transcription by an unknown mechanism operating without obvious changes in epigenetic marks. We have isolated an enhancer of the mom1 mutation that points towards regulatory interplay between MOM1 and the plant-specific RNA Polymerase V (Pol V). Pol V transcribes heterochromatic loci and silences them. Although its biochemical properties have been studied; it is still not clear how Pol V is targeted to heterochromatin. We now provide evidence that Pol V is required for MOM1-mediated suppression of transcription at a subset of its chromosomal targets. Thus, Pol V interacts with MOM1 in the control of gene silencing. Interestingly, functional relationships between mutations in MOM1 and Pol V genes range from enhancement to independence or even suppression at different target loci. 4 samples: wt, mom1, nrpe1, mom/nrpe1 with 3 replicates each
2010-06-19 | E-GEOD-17940 | biostudies-arrayexpress
Project description:Heterochromatin is an inert region in the genome and composed of mainly remnants of transposons and repetitive elements. In Arabidopsis, the major heterchromatin regions are present at around centromeres (pericentromeric regions) and at a region on the short arm of chromosome 4 (heterochromatin knob). Histones and DNAs in heterochromatin have characteristic features with abundant H3H9me2 and cytosine methylation, respectively. Here, by using a genome tiling array, we showed that a subset of heterochromatin loci are silenced by the action of Morpheus' molecule 1 (MOM1) that is an epigeneic regulator for transcriptional gene silencing independent of global DNA and histone modification. Most of the up-regulated loci in the mom1 mutant carried sequences related to transposable elements but none of them was annotated as functional transposons. No specific subclass of transposons was targeted by MOM1 and loci that were unrelated to transposons but flanked by short tandem repeats were also shown to be under the control of MOM1. The results suggest the presence of an unknown level of regulatory network maintaining the silent state of heterochromain in the genome. Keywords: Epigenetic regulation of endogenous loci by Morpheus' Molecule 1 (MOM1)
2010-09-27 | GSE13092 | GEO
Project description:Heterochromatin is an inert region in the genome and composed of mainly remnants of transposons and repetitive elements. In Arabidopsis, the major heterchromatin regions are present at around centromeres (pericentromeric regions) and at a region on the short arm of chromosome 4 (heterochromatin knob). Histones and DNAs in heterochromatin have characteristic features with abundant H3H9me2 and cytosine methylation, respectively. Here, by using a genome tiling array, we showed that a subset of heterochromatin loci are silenced by the action of Morpheus' molecule 1 (MOM1) that is an epigeneic regulator for transcriptional gene silencing independent of global DNA and histone modification. Most of the up-regulated loci in the mom1 mutant carried sequences related to transposable elements but none of them was annotated as functional transposons. No specific subclass of transposons was targeted by MOM1 and loci that were unrelated to transposons but flanked by short tandem repeats were also shown to be under the control of MOM1. The results suggest the presence of an unknown level of regulatory network maintaining the silent state of heterochromain in the genome. Keywords: Epigenetic regulation of endogenous loci by Morpheus' Molecule 1 (MOM1) Three-week-old Arabidopsis plants (Col-0 and mom1-2) grown on soil were subjected to RNA extraction and the total RNA samples were used for the microarray hybridization. Three replicative hybridization experiments for each strand array were carried out using the independent biological RNA samples.
2010-09-26 | E-GEOD-13092 | biostudies-arrayexpress
Project description:In plants, RNA-directed DNA methylation (RdDM) pathway is a well-known de novo DNA methylation pathway that is involved in many important biological processes, such as pathogen defense, stress response and plant development. RdDM involves two plant-specific RNA polymerases, Pol IV and Pol V. In previous studies, several genetic screen systems, including a release of silencing 1 (ros1) suppressor screen, have been designed and used to discover new RdDM components. Through the ros1 suppressor screen, several new RdDM components, such as RDM1 and KTF1, have been reported. In this study, we isolated a new ros1 suppressor mutant, rdm15. Through DNA methylome and whole-genome siRNA analyses, we showed that RDM15 was required for RdDM-dependent DNA methylation and siRNA accumulation at a subset of RdDM target loci. Our further investigation revealed that RDM15 mainly contributes to Pol V-dependent downstream siRNA accumulation, and can interact with NRPE3B, a subunit specific to Pol V. DNA methylation and histone modifications are known to interact with each other to determine DNA methylation and chromatin states. Here, we showed that RDM15 can specifically recognize the histone 3 lysine 4 monomethylation (H3K4me1) mark by its C-terminal tudor domain. The structure of RDM15 tudor domain in complex with an H3K4me1 peptide highlights the specific recognition of H3K4me1 by an aromatic cage and specific hydorgen bonding interactions, which is different from all previously reported lower methyllysine recognition mechanisms. In addition, at the genome wide level, RDM15 and H3K4me1 showed similar distribution patterns at RDM15-dependent RdDM loci, suggesting that RDM15 recognition of H3K4me1 is associated with RDM15 function in RdDM. In summary, we identified and characterized a histone H3K4me1 specific binding protein as a new RdDM component, and the structural analysis of RDM15 revealed a new type of chemical feature-based lower methyllysine recognition mechanism.
2021-03-08 | GSE154302 | GEO
Project description:The mechanism by which MORPHEUS'MOLECULE1 (MOM1) contributes to transcriptional gene silencing remained elusive since the gene was first identified and characterized (Amedeo et al., 2000). Here, we report that two PIAS (PROTEIN INHIBITOR OF ACTIVATED STAT)-type SUMO E3 ligase-like proteins PIAL1 and PIAL2 function redundantly to mediate transcriptional silencing at MOM1 target loci. PIAL1 and PIAL2 physically interact with each other and with MOM1 to form a high-molecular-weight complex. In the absence of either PIAL2 or MOM1, the formation of the high-molecular-weight complex was disrupted. We identified a previously uncharacterized IND (interacting domain) in PIAL1 and PIAL2, and demonstrated that IND directly interacts with MOM1. The CMM2 (conserved MOM1 motif 2) domain of MOM1 was previously shown to be required for the dimerization of MOM1. We demonstrated that the CMM2 domain is also required for the interaction of MOM1 with PIAL1 and PIAL2. We found that although PIAL2 has a SUMO E3 ligase activity, the activity is dispensable for PIAL2 in transcriptional silencing. This study suggests that PIAL1 and PIAl2 act as components of the MOM1-containing complex to mediate transcriptional silencing at heterochromatin regions.
2016-04-15 | GSE80302 | GEO
Project description:The mechanism by which MORPHEUS'MOLECULE1 (MOM1) contributes to transcriptional gene silencing remained elusive since the gene was first identified and characterized (Amedeo et al., 2000). Here, we report that two PIAS (PROTEIN INHIBITOR OF ACTIVATED STAT)-type SUMO E3 ligase-like proteins PIAL1 and PIAL2 function redundantly to mediate transcriptional silencing at MOM1 target loci. PIAL1 and PIAL2 physically interact with each other and with MOM1 to form a high-molecular-weight complex. In the absence of either PIAL2 or MOM1, the formation of the high-molecular-weight complex was disrupted. We identified a previously uncharacterized IND (interacting domain) in PIAL1 and PIAL2, and demonstrated that IND directly interacts with MOM1. The CMM2 (conserved MOM1 motif 2) domain of MOM1 was previously shown to be required for the dimerization of MOM1. We demonstrated that the CMM2 domain is also required for the interaction of MOM1 with PIAL1 and PIAL2. We found that although PIAL2 has a SUMO E3 ligase activity, the activity is dispensable for PIAL2 in transcriptional silencing. This study suggests that PIAL1 and PIAl2 act as components of the MOM1-containing complex to mediate transcriptional silencing at heterochromatin regions.
2016-04-15 | GSE80301 | GEO