COMPASS complexes redundantly regulate gene expression and DNA methylation in Arabidopsis [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA851768 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19784269_1.fastq.gz | Fastqsanger.gz | |||
| SRR19784269_2.fastq.gz | Fastqsanger.gz | |||
| SRR19784270_1.fastq.gz | Fastqsanger.gz | |||
| SRR19784270_2.fastq.gz | Fastqsanger.gz | |||
| SRR19784271_1.fastq.gz | Fastqsanger.gz |
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Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206685 | GEO
Project description:COMPASS complexes redundantly regulate gene expression and DNA methylation in Arabidopsis
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Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206683 | GEO
Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206687 | GEO
Project description:COMPASS complexes redundantly regulate gene expression and DNA methylation in Arabidopsis [Bisulfite-seq]
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Project description:COMPASS complexes redundantly regulate gene expression and DNA methylation in Arabidopsis [RNA-seq]
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Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation. ChIP-Seq experiments were performed on Illumina HiScanSQ sequencer in wild-type HEK293T cells for H3K4me3 histone marks, O-GlcNAc and HCF1, for HT-TET2, HT-TET3 and HT-OGT in HEK293T cells overexpressing those three fusion proteins and in TET2 Kd HEK293T cells for H3K4me3 histone marks. ChIP-Seqs were also performed in mouse bone marrow tissues for H3K4me3 histone marks, O-GlcNAc, endogenous Tet2 and in Tet2 Ko bone marrow tissues for H3K4me3 histone marks.
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