Multivalent H3K9me2 Reader ADCP1 Functions as a plant HP1 to Maintain Epigenetic Silencing
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ABSTRACT:
PROVIDER: PRJNA484219 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7639970_1.fastq.gz | Fastqsanger.gz | |||
| SRR7639970_2.fastq.gz | Fastqsanger.gz | |||
| SRR7639980_1.fastq.gz | Fastqsanger.gz | |||
| SRR7639980_2.fastq.gz | Fastqsanger.gz | |||
| SRR7639990_1.fastq.gz | Fastqsanger.gz |
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Project description:Heterochromatin formation is important for genome stability and transposon silencing. The evolutionally conserved Heterochromatin Protein 1 (HP1) recognizes H3K9me3 and maintains heterochromatin from fission yeast to mammalians. However, it is still questioned about the presence of HP1 protein in plants. Here, we discovered a multivalent H3K9me2 reader ADCP1 in Arabidopsis through biophysical and structural studies, and agenet domain in ADCP1 has the similar function of chromo domain in HP1. We further showed that ADCP1 was essential for heterochromatin maintenance through modulating H3K9me2 and DNA methylation levels. Similar to human HP1alpha and fly HP1a, ADCP1 was also able to mediate heterochromatin phase separation both in vitro and in vivo. Our results demonstrate the plant specific and evolution conserved ADCP1 functions as the HP1 equivalent protein in plant.
2018-11-15 | GSE118063 | GEO
Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
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Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
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Project description:Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well conserved epigenetic silencing mark and its reader molecule, and crucial for heterochromatin formation. However, the details of the importance of H3K9 methylation and HP1 in heterochromatin formation still remain unclear. One of the reason is the redundancy problem, as there are multiple reader molecules for H3K9 methylation, including HP1, and HP1 itself functions as a hub that recruits various effector molecules. To overcome the redundancy issue, we took synthetic biology approach and introduced H3K9 methylation and HP1 into budding yeast Saccharomyces cerevisiae, which does not have this system, and examined its impact on transcription and chromatin compaction. We observed that mammalian H3K9 methyltransferase can induce genome wide H3K9 di- and tri-methylation (H3K9me2,3) in budding yeast, and that HP1 accumulates over the H3K9 methylated regions. However, H3K9 methylation occurred mainly in the gene body region of the genes and excluded around TSS where H3K9ac pre-exists. Correspondingly, expression of H3K9 methyltransferase and HP1 did not affect transcription in budding yeast, including repression. ATAC-seq analysis also showed no impact on chromatin accessibility, and Hi-C-seq analysis of chromatin 3D structure revealed no significant differences. These results suggest that even though H3K9 methylation and recruitment of HP1 play essential roles in epigenetic regulation of heterochromatin, they are not sufficient to build up heterochromatin, at least at gene body regions, and further participation of effector molecules, including downstream factors of HP1, is required.
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Project description:Chromatin landscape of budding yeast acquiring H3K9 methylation and its reader molecule HP1
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Project description:In this article, we first obtained HP1 triple-knockout embryonic stem cells using Crispr-Cas9 and Cre-loxP systems. At the same time, we also obtained single-knock and double-knock cell lines respectively. On this basis, we studied The function of HP1 in embryonic stem cells was found to have a very important role in the regulation of differentiation and reproduction-related genes.In our follow-up study, we found that the deletion of HP1 leads to the differentiation tendency of embryonic stem cells into endoderm. Considering that HP1 has an important function of H3K9me3 recognition and binding, we examined the effect of HP1 deletion on histone modifications, we found that H3K9me2 and H3K9me3 modifications were significantly reduced, and then through rescue experiments, we thought that HP1 may be through OCT4 and NANOG and then further functional.
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