Expression data from leaf of Arabidopsis TGS mutants
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE5771 | GEO | 2007/08/29
SECONDARY ACCESSION(S): PRJNA97115
REPOSITORIES: GEO
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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
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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.
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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.
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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, again colocalized with MORC6. These findings demonstrate a multifaceted role of MOM1 in genome regulation.
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Project description:Epigenetic gene silencing is of central importance to maintain genome integrity and is mediated by an elaborate interplay between DNA methylation, histone posttranslational modifications and chromatin remodeling complexes. DNA methylation and repressive histone marks usually correlate with transcriptionally silent heterochromatin, however there are exceptions to this interdependence. In Arabidopsis, mutation of MORPHEUS MOLECULE 1 (MOM1) causes transcriptional derepression of heterochromatin independently of changes in DNA methylation. More recently, two Arabidopsis homologs of mouse Microrchidia (MORC) have also been implicated in gene silencing and heterochromatin condensation without altering genome-wide DNA methylation patterns. In this study, we show that AtMORC6 physically interacts with AtMORC1 and with its close homologue AtMORC2 in two mutually exclusive protein complexes. RNA-seq analysis of high-order mutants indicates that AtMORC1 and AtMORC2 act redundantly to repress a common set of loci. We also examined the genetic interactions between AtMORC6 and MOM1 pathways. Although AtMORC6 and MOM1 control the silencing of a very similar set of genomic loci, we observed synergistic transcriptional regulation in the mom1/atmorc6 double mutant, suggesting that these epigenetic regulators act mainly by independent silencing mechanisms. RNA-seq libraries were prepared for two suites of mutants to allow direct comparisons between mutants within each set. The two sets consisted of the following samples: Set_1) A wildtype (Col) control, the morc1 mutant, the morc2 mutant, the morc1 morc2 double mutant, the morc6 mutant, and the morc1 morc2 morc6 triple mutant ; Set_2) A wildtpe (Col) control, the morc6 mutant, the mom1 mutant, and the mom1 morc6 double mutant. For each sample, two biological replicates were performed (denoted "bio_replicate_1" or "bio_replicate_2"). Whole genome bisulifte libraries were sequenced from material grown in parallel.
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Project description:Epigenetic gene silencing is of central importance to maintain genome integrity and is mediated by an elaborate interplay between DNA methylation, histone posttranslational modifications and chromatin remodeling complexes. DNA methylation and repressive histone marks usually correlate with transcriptionally silent heterochromatin, however there are exceptions to this interdependence. In Arabidopsis, mutation of MORPHEUS MOLECULE 1 (MOM1) causes transcriptional derepression of heterochromatin independently of changes in DNA methylation. More recently, two Arabidopsis homologs of mouse Microrchidia (MORC) have also been implicated in gene silencing and heterochromatin condensation without altering genome-wide DNA methylation patterns. In this study, we show that AtMORC6 physically interacts with AtMORC1 and with its close homologue AtMORC2 in two mutually exclusive protein complexes. RNA-seq analysis of high-order mutants indicates that AtMORC1 and AtMORC2 act redundantly to repress a common set of loci. We also examined the genetic interactions between AtMORC6 and MOM1 pathways. Although AtMORC6 and MOM1 control the silencing of a very similar set of genomic loci, we observed synergistic transcriptional regulation in the mom1/atmorc6 double mutant, suggesting that these epigenetic regulators act mainly by independent silencing mechanisms.
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