The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status
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ABSTRACT:
PROVIDER: PRJNA255871 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1522110.fastq.gz | Fastqsanger.gz | |||
| SRR1522111.fastq.gz | Fastqsanger.gz | |||
| SRR3707330.fastq.gz | Fastqsanger.gz | |||
| SRR3707340.fastq.gz | Fastqsanger.gz | |||
| SRR3707331.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:DNA methylation is a chromatin modification that is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation have been identified, relatively little is understood about how DNA methylation influences gene expression. Using complementary genetic and biochemical approaches we identified a protein complex that antagonizes the transcriptional gene silencing of two LUCIFERASE (LUC) reporters in a manner that requires DNA methylation. At its core, this complex contains LOW IN LUCIFERASE EXPRESSION (LIL), an α-crystallin domain protein, and METHYL-CpG-BINDING DOMAIN 7 (MBD7), a protein previously associated with DNA methylation. At the LUC reporters, loss of MBD7 or LIL resulted in decreased LUC expression concomitant with modest, but reproducible increases in DNA methylation that can be phenocopied by DNA demethylase mutants. These findings are consistent with other reports and reveal a genetic connection between MBD7, LIL and DNA demethylation. However, we found that the hyper-methylation and gene expression phenotypes at a LUC reporter can be genetically uncoupled, demonstrating that changes in DNA methylation alone are not sufficient to silence LUC expression, and suggesting a role for the MBD7-LIL complex downstream of DNA methylation. Consistent with this hypothesis, our more extensive analysis of DNA methylation in mbd7 and lil mutants revealed only a small number of hyper-methylated loci genome wide. Furthermore, these loci displayed minimal overlap with demethylase targets, suggesting that, in general, the DNA demethylation machinery does not function in a manner dependent on the MBD7-LIL complex. Taken together, our findings place the MBD7-LIL complex amongst a small number of factors that regulate gene expression without causing significant changes in DNA methylation. This complex, however, is unique in that it functions to suppress, rather than enforce the silencing effects of DNA methylation, enabling gene expression of several transgene reporters despite high levels of promoter methylation.
2017-04-26 | GSE83355 | GEO
Project description:DNA methylation is a chromatin modification that is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation have been identified, relatively little is understood about how DNA methylation influences gene expression. Using complementary genetic and biochemical approaches we identified a protein complex that antagonizes the transcriptional gene silencing of two LUCIFERASE (LUC) reporters in a manner that requires DNA methylation. At its core, this complex contains LOW IN LUCIFERASE EXPRESSION (LIL), an α-crystallin domain protein, and METHYL-CpG-BINDING DOMAIN 7 (MBD7), a protein previously associated with DNA methylation. At the LUC reporters, loss of MBD7 or LIL resulted in decreased LUC expression concomitant with modest, but reproducible increases in DNA methylation that can be phenocopied by DNA demethylase mutants. These findings are consistent with other reports and reveal a genetic connection between MBD7, LIL and DNA demethylation. However, we found that the hyper-methylation and gene expression phenotypes at a LUC reporter can be genetically uncoupled, demonstrating that changes in DNA methylation alone are not sufficient to silence LUC expression, and suggesting a role for the MBD7-LIL complex downstream of DNA methylation. Consistent with this hypothesis, our more extensive analysis of DNA methylation in mbd7 and lil mutants revealed only a small number of hyper-methylated loci genome wide. Furthermore, these loci displayed minimal overlap with demethylase targets, suggesting that, in general, the DNA demethylation machinery does not function in a manner dependent on the MBD7-LIL complex. Taken together, our findings place the MBD7-LIL complex amongst a small number of factors that regulate gene expression without causing significant changes in DNA methylation. This complex, however, is unique in that it functions to suppress, rather than enforce the silencing effects of DNA methylation, enabling gene expression of several transgene reporters despite high levels of promoter methylation.
2017-05-05 | GSE83557 | GEO
Project description:DNA methylation is a chromatin modification that is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation have been identified, relatively little is understood about how DNA methylation influences gene expression. Using complementary genetic and biochemical approaches we identified a protein complex that antagonizes the transcriptional gene silencing of two LUCIFERASE (LUC) reporters in a manner that requires DNA methylation. At its core, this complex contains LOW IN LUCIFERASE EXPRESSION (LIL), an α-crystallin domain protein, and METHYL-CpG-BINDING DOMAIN 7 (MBD7), a protein previously associated with DNA methylation. At the LUC reporters, loss of MBD7 or LIL resulted in decreased LUC expression concomitant with modest, but reproducible increases in DNA methylation that can be phenocopied by DNA demethylase mutants. These findings are consistent with other reports and reveal a genetic connection between MBD7, LIL and DNA demethylation. However, we found that the hyper-methylation and gene expression phenotypes at a LUC reporter can be genetically uncoupled, demonstrating that changes in DNA methylation alone are not sufficient to silence LUC expression, and suggesting a role for the MBD7-LIL complex downstream of DNA methylation. Consistent with this hypothesis, our more extensive analysis of DNA methylation in mbd7 and lil mutants revealed only a small number of hyper-methylated loci genome wide. Furthermore, these loci displayed minimal overlap with demethylase targets, suggesting that, in general, the DNA demethylation machinery does not function in a manner dependent on the MBD7-LIL complex. Taken together, our findings place the MBD7-LIL complex amongst a small number of factors that regulate gene expression without causing significant changes in DNA methylation. This complex, however, is unique in that it functions to suppress, rather than enforce the silencing effects of DNA methylation, enabling gene expression of several transgene reporters despite high levels of promoter methylation.
2017-05-05 | GSE59639 | GEO
Project description:DNA methylation is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation are known, relatively little is understood about how DNA methylation influences gene expression. Here we identified a METHYL-CpG-BINDING DOMAIN 7 (MBD7) complex in Arabidopsis thaliana that suppresses the transcriptional silencing of two LUCIFERASE (LUC) reporters via a mechanism that is largely downstream of DNA methylation. Although mutations in components of the MBD7 complex resulted in modest increases in DNA methylation concomitant with decreased LUC expression, we found that these hyper-methylation and gene expression phenotypes can be genetically uncoupled. This finding, along with genome-wide profiling experiments showing minimal changes in DNA methylation upon disruption of the MBD7 complex, places the MBD7 complex amongst a small number of factors acting downstream of DNA methylation. This complex, however, is unique as it functions to suppress, rather than enforce, DNA methylation-mediated gene silencing.
| S-EPMC5462541 | biostudies-literature
Project description:The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status
| PRJNA325663 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-05-05 | GSE59658 | GEO
Project description:The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status (mRNA-seq)
| PRJNA326338 | ENA
Project description:The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status (smallRNA-seq)
| PRJNA255870 | ENA
Project description:MBD5, MBD6, and MBD7 are CG-specific methyl-readers with opposite functions: MBD5 and MBD6 (MBD5/6) redundantly repress methylated loci in pollen vegetative nuclei (VN), while MBD7 prevents transgene silencing, possibly by promoting DNA demethylation. Here we show that transcriptional derepression in mbd5/6 pollen is rescued by loss of MBD7, suggesting that MBD5/6 counteract MBD7 activity. By simultaneously profiling DNA methylation and gene expression in single pollen nuclei, we found that CG methylation is lost at MBD5/6 targets specifically in the early post-mitotic VN of mbd5/6. This loss precedes mbd5/6 transcriptional derepression and is largely restored in mbd5/6/7 triple mutants. Altering MBD6 to recruit the MBD7 complex instead of its normal interactors caused demethylation and upregulation of MBD5/6 targets, turning MBD6 from a repressor into an activator. We propose that in VN, where chromatin is decondensed, MBD5/6 are required to protect accessible DNA from demethylation and derepression by the MBD7 complex.
2025-11-13 | GSE275698 | GEO
Project description:In eukaryotes, heterochromatin is characterized by numerous epigenetic marks, including DNA methylation. Spreading of these marks into nearby active genes must be avoided in order to maintain appropriate gene expression. Here, we uncover Arabidopsis Methyl-CpG-Binding Domain 7 (MBD7) and Increased DNA Methylation 3 (IDM3) as anti-silencing factors that prevent transgene repression and genome-wide DNA hypermethylation. MBD7 preferentially binds to highly methylated, CG-dense regions associated with non-CG methylation and physically associates with other anti-silencing factors, including the histone acetyltransferase IDM1, IDM2, and IDM3. IDM1 and IDM2 were previously shown to facilitate active DNA demethylation by the 5-methylcytosine DNA glycosylase/lyase ROS1. Thus, MBD7 tethers the IDM proteins to methylated DNA, which enables the function of DNA demethylases that in turn establish chromatin boundaries and limit DNA methylation Using ChIP-seq to study the genomic targeting principle of MBD7 protein Examination of MBD7 protein binding principle using ChIP-Seq. WT and proMBD7::gMBD7::4xMYC transgenic plants were used for ChIP-seq.
2015-01-29 | E-GEOD-58789 | biostudies-arrayexpress