Major alleles of CDCA7α shape CG-methylation in Arabidopsis thaliana [WGBS]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1196491 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31670100_1.fastq.gz | Fastqsanger.gz | |||
| SRR31670100_2.fastq.gz | Fastqsanger.gz | |||
| SRR31670101_1.fastq.gz | Fastqsanger.gz | |||
| SRR31670101_2.fastq.gz | Fastqsanger.gz | |||
| SRR31670102_1.fastq.gz | Fastqsanger.gz |
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Project description:DNA methylation is a key epigenetic mark that impacts gene expression and represses transposable elements (TEs) in eukaryotes. Numerous examples of cis-elements targeted by DNA methylation, particularly at CG sites (mCG), have been reported to be under selective pressure in animals and plants. By contrast, there is limited knowledge of trans-regulators of mCG leading to adaptation. Here, using genome-wide association studies, we identify CELL DIVISION CYCLE-ASSOCIATED PROTEIN 7 ALPHA (CDCA7α) as a trans-regulator of mCG in natural populations of Arabidopsis thaliana. CDCA7α and its paralog, CDCA7β, directly bind to the chromatin remodeler DECREASE IN DNA METHYLATION 1 (DDM1), which facilitates access of methyltransferases to DNA. CDCA7α/β selectively regulates mCG and minimally impacts other DDM1-dependent processes such as non-CG methylation and histone variant deposition. We identify the cis-regulatory sequence modulating CDCA7α expression in natural populations and determining the degree of mCG and TE silencing. The geographic distribution of CDCA7α alleles suggests that new alleles have repeatedly expanded to novel ecological niches, indicating a potential role in local adaptation. Altogether, our findings provide new insight into how changes in global DNA methylation levels through transcriptional regulation of the epigenetic machinery have the capacity to facilitate local adaptation.
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Project description:Major alleles of CDCA7α shape CG-methylation in Arabidopsis thaliana [ChIP-Seq]
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Project description:Major alleles of CDCA7α shape CG-methylation in Arabidopsis thaliana [RNA-seq]
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Project description:DNA methylation is a key epigenetic mark that impacts gene expression and represses transposable elements (TEs) in eukaryotes. Numerous examples of cis-elements targeted by DNA methylation, particularly at CG sites (mCG), have been reported to be under selective pressure in animals and plants. By contrast, there is limited knowledge of trans-regulators of mCG leading to adaptation. Here, using genome-wide association studies, we identify CELL DIVISION CYCLE-ASSOCIATED PROTEIN 7 ALPHA (CDCA7α) as a trans-regulator of mCG in natural populations of Arabidopsis thaliana. CDCA7α and its paralog, CDCA7β, directly bind to the chromatin remodeler DECREASE IN DNA METHYLATION 1 (DDM1), which facilitates access of methyltransferases to DNA. CDCA7α/β selectively regulates mCG and minimally impacts other DDM1-dependent processes such as non-CG methylation and histone variant deposition. We identify the cis-regulatory sequence modulating CDCA7α expression in natural populations and determining the degree of mCG and TE silencing. The geographic distribution of CDCA7α alleles suggests that new alleles have repeatedly expanded to novel ecological niches, indicating a potential role in local adaptation. Altogether, our findings provide new insight into how changes in global DNA methylation levels through transcriptional regulation of the epigenetic machinery have the capacity to facilitate local adaptation.
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Project description:DNA methylation is a key epigenetic mark that impacts gene expression and represses transposable elements (TEs) in eukaryotes. Numerous examples of cis-elements targeted by DNA methylation, particularly at CG sites (mCG), have been reported to be under selective pressure in animals and plants. By contrast, there is limited knowledge of trans-regulators of mCG leading to adaptation. Here, using genome-wide association studies, we identify CELL DIVISION CYCLE-ASSOCIATED PROTEIN 7 ALPHA (CDCA7α) as a trans-regulator of mCG in natural populations of Arabidopsis thaliana. CDCA7α and its paralog, CDCA7β, directly bind to the chromatin remodeler DECREASE IN DNA METHYLATION 1 (DDM1), which facilitates access of methyltransferases to DNA. CDCA7α/β selectively regulates mCG and minimally impacts other DDM1-dependent processes such as non-CG methylation and histone variant deposition. We identify the cis-regulatory sequence modulating CDCA7α expression in natural populations and determining the degree of mCG and TE silencing. The geographic distribution of CDCA7α alleles suggests that new alleles have repeatedly expanded to novel ecological niches, indicating a potential role in local adaptation. Altogether, our findings provide new insight into how changes in global DNA methylation levels through transcriptional regulation of the epigenetic machinery have the capacity to facilitate local adaptation.
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Project description:Genetic neuroscience: How human genes and alleles shape neuronal phenotypes
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Project description:Genetic neuroscience: How human genes and alleles shape neuronal phenotypes
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Project description:DNA methylation occurs in both CG and non-CG sequence contexts. Non-CG methylation is abundant in plants, and is mediated by CHROMOMETHYLASE (CMT) and DOMAINS REARRANGED METHYLTRANSFERASE (DRM) proteins; however its roles remain poorly understood. Here we characterize the roles of non-CG methylation in Arabidopsis thaliana. We show that a poorly characterized methyltransferase, CMT2, is a functional methyltransferase in vitro and in vivo. CMT2 specifically binds histone H3 lysine 9 (H3K9) dimethylation and methylates non-CG cytosines at sites that are also regulated by H3K9 dimethylation. By generating different combinations of non-CG methylation mutants, we reveal the contributions and redundancies between each methyltransferase in DNA methylation patterning and in regulating transposable elements (TEs) and protein-coding genes. We also demonstrate extensive dependencies of small RNA accumulation and H3K9 methylation patterning on non-CG methylation, suggesting self-reinforcing mechanisms between these epigenetic factors. The results suggest that non-CG methylation patterns are critical in shaping the histone modification and small non-coding RNA landscapes.
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Project description:During postnatal development the DNA methyltransferase DNMT3A deposits high levels of nonCG cytosine methylation in neurons. This unique methylation is critical for transcriptional regulation in the mature mammalian brain, and loss of this mark is implicated in DNMT3Aassociated neurodevelopmental disorders (NDDs). The mechanisms determining genomic nonCG methylation profiles are not well defined however, and it is unknown if this pathway is disrupted in additional NDDs. Here we show that genome topology and gene-expression converge to shape Histone H3 lysine 36 dimethylation (H3K36me2) profiles, which in turn recruit DNMT3A and pattern neuronal non-CG methylation. Brain-specific deletion of NSD1, the H3K36 methyltransferase mutated in the NDD Sotos syndrome, disrupts megabase-scale H3K36me2 patterns, causing alterations in non-CG methylation and transcription that overlap models of DNMT3A disorders. Our findings indicate that H3K36me2 deposited by NSD1 is an important determinant of neuronal non-CG DNA methylation and implicates disruption of this methylation in Sotos syndrome.
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