Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146353 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR349697.fastq.gz | Fastqsanger.gz | |||
| SRR349698.fastq.gz | Fastqsanger.gz | |||
| SRR349699.fastq.gz | Fastqsanger.gz | |||
| SRR349700.fastq.gz | Fastqsanger.gz |
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Project description:The small RNA mediated DNA methylation (RdDM) is highly elaborated in Arabidopsis as an important epigenetic pathway controls expression of genes and multiple developmental processes. RDR2 and DCL3 are necessary factors to the 24-nt siRNA biogenesis and the RdDM pathway. Here, we find that IBM1 (increase in BONSAI methylation 1), a conserved JmjC family histone demethylase, could directly associated with the chromatin of RDR2 and DCL3. The IBM1 mutation induces hypermethylation on both H3K9 and DNA non-CG sites in these loci, and further represses their expression. The reduction of RDR2 and DCL3 may affect siRNA biogenesis in a locus-specific manner and disrupt the RdDM directed repression. It suggests an indirect way to regulate targets by IBM1 through control of siRNA biogenesis, and demonstrate the relationship between histone methylation and small RNAs. Genome-wide integrated mapping of mRNA transcripts and small RNAs, using whole plant of 10-days seedlings of the Columbia-0 wildtype and ibm1-3 mutant Arabidopsis thaliana.
2012-08-03 | E-GEOD-32284 | biostudies-arrayexpress
Project description:The small RNA mediated DNA methylation (RdDM) is highly elaborated in Arabidopsis as an important epigenetic pathway controls expression of genes and multiple developmental processes. RDR2 and DCL3 are necessary factors to the 24-nt siRNA biogenesis and the RdDM pathway. Here, we find that IBM1 (increase in BONSAI methylation 1), a conserved JmjC family histone demethylase, could directly associated with the chromatin of RDR2 and DCL3. The IBM1 mutation induces hypermethylation on both H3K9 and DNA non-CG sites in these loci, and further represses their expression. The reduction of RDR2 and DCL3 may affect siRNA biogenesis in a locus-specific manner and disrupt the RdDM directed repression. It suggests an indirect way to regulate targets by IBM1 through control of siRNA biogenesis, and demonstrate the relationship between histone methylation and small RNAs.
2012-08-03 | GSE32284 | GEO
Project description:n Arabidopsis and other species, anthocyanin accumulation specifically depends on light signaling. The CONSTITUTIVELY PHOTOMORPHOGENIC1/SUPPRESSOR OF PHYA-105 (COP1/SPA) complex is required for the control of anthocyanin biosynthesis in response to light, but the precise mechanism underlying this process is largely unknown. Here we report that Increase in BONSAI Methylation 1 (IBM1), a JmjC domain-containing histone demethylase, participates in the regulation of light-induced anthocyanin biosynthesis in Arabidopsis. Loss-of-function mutations of IBM1 lead to accelerated anthocyanin accumulation in high light. We further identified that IBM1 is directly associated with SPA1/2/3 chromatin in vivo, whereas knockout of IBM1 resulted in an elevated level of H3K9 methylation and DNA non-CG sites within SPA genes, thereby repressing their expression. Transgenic ibm1 plants overexpressing SPA1demonstrated that SPA1 was capable of complementing the mutant phenotype. Our results reveal a novel mechanism that controls the epigenetic regulation of anthocyanin biosynthesis and offer insight into how plant adapt to high light stress. This study could contribute to a better understanding of the linkage between light signaling and anthocyanin biosynthesis in plants
2018-03-01 | GSE106568 | GEO
Project description:Histone methylation plays important roles in the regulation of chromatin dynamics and transcription. Steady state levels of histone lysine methylation are regulated by a balance between enzymes that catalyze either the addition or removal of methyl groups. Using an activity-based biochemical approach, we recently uncovered the JmjC domain as an evolutionarily conserved signature motif for histone demethylases. Furthermore, we demonstrated that Jhd1, a JmjC domain-containing protein in S. cerevisiae, is an H3K36-specific demethylase. Here we report further characterization of Jhd1. Similar to its mammalian homolog, Jhd1-catalyzed histone demethylation requires iron and alpha-ketoglutarate as cofactors. Mutation and deletion studies indicate that the JmjC domain and adjacent sequences are critical for Jhd1 enzymatic activity, while the N-terminal PHD domain is dispensable. Overexpression of JHD1 results in a global reduction of H3K36 methylation in vivo. Finally, chromatin immunoprecipitation coupled microarray (ChIP-chip) studies reveal subtle changes in the distribution of H3K36me2 upon overexpression or deletion of JHD1. Our studies establish Jhd1 as a histone demethylase in budding yeast and suggest that Jhd1 functions to maintain the fidelity of histone methylation patterns along transcription units. Keywords: ChIP-chip H3K36me2 ChIPs were performed on wild type, jhd1 knockout, and JHD1 overexpression yeast strains.
2010-06-11 | E-GEOD-7627 | biostudies-arrayexpress
Project description:Transposable elements (TEs) make up a large proportion of eukaryotic genomes. As their mobilization creates genetic variation that threatens genome integrity, TEs are epigenetically silenced through several pathways and this may spread to neighboring sequences. JUMONJI (JMJ) proteins can function as anti-silencing factors and prevent silencing of genes next to TEs. Whether TE silencing is counterbalanced by the activity of anti-silencing factors is still unclear. Here, we characterize JMJ24 as a regulator of TE silencing. We show that loss of JMJ24 results in increased silencing of the DNA transposon AtMu1c, while overexpression of JMJ24 reduces silencing. JMJ24 has a JumonjiC (JmjC) domain and two RING domains. JMJ24 auto-ubiquitinates in vitro, demonstrating E3 ligase activity of the RING domain(s). JMJ24-JmjC binds the N-terminal tail of histone H3 and full-length JMJ24 binds histone H3 in vivo. JMJ24 activity is anti-correlated with histone H3 lysine 9 dimethylation (H3K9me2) levels at AtMu1c. Double mutant analyses with epigenetic silencing mutants suggest that JMJ24 antagonizes histone H3K9me2, and requires H3K9 methyltransferases for its activity on AtMu1c. Genome-wide transcriptome analysis indicates that JMJ24 affects silencing at additional TEs. Our results suggest that the JmjC domain of JMJ24 has lost demethylase activity but has been retained as a binding domain for histone H3. This is in line with phylogenetic analyses indicating that JMJ24 [with the mutated JmjC domain] is widely conserved in angiosperms. Taken together, this study assigns a role in TE silencing to a conserved JmjC-domain protein with E3 ligase activity, but no demethylase activity.
2016-03-18 | GSE72954 | GEO
Project description:In plants, the biogenesis of 24 nt and 23 nt small interfering RNAs (siRNAs) requires NUCLEAR RNA POLYMERASE IV (Pol IV), RNA-DEPENDENT RNA POLYMERASE 2 (RDR2) and DICER-LIKE 3 (DCL3). We show that single-stranded M13 bacteriophage DNA can be used as a template for siRNA synthesis in vitro. Deep sequencing of RNAs produced from the in vitro reactions of Pol IV, RDR2 and DCL3 shows that Pol IV transcribes the DNA into first-strand RNAs which RDR2 then uses as templates to synthesize complementary second strands. These siRNA precursor transcripts made by Pol IV and RDR2 are mostly 30-50 nt. An untemplated 3' terminal nucleotide is a characteristic of RDR2 transcripts. DCL3 dicing of double-stranded precursor RNAs synthesized by Pol IV and RDR2 generates siRNAs that are mostly 24 nt, with a smaller population of 23 nt also produced.
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Project description:Retrotransposons are classified into long terminal repeat (LTR) or non-LTR retrotransoposons, and both types can mobilize in a “copy and paste” manner. Rice genome contains >40% of repetitive sequences or transposable elements (TEs) that scattered throughout the genome. TE activities are tightly regulated by distinct epigenetic mechanisms. Histone lysine methylation is catalyzed by SET domain group (SDG) protein and reversed by a family of Jumonji C (JmjC) domain-containing proteins. In rice, DNA methylation and histone methylation have been implicated in controlling copia-like LTR retrotransposon Tos17 activities. Whether any TEs are controlled by histone demethylase remains to be elusive. Here, we show that JMJ703 is a histone H3K4 specific demethylase in rice. Impaired JMJ703 disrupted genome-wide transcriptome and enhanced H3K4me3 resulting in pleiotropic defects. Two LINE elements, Karma and its N-terminal truncation were identified as direct targets of JMJ703 with increased frequency of transposition in jmj703, while Tos17 is unaffected. Our findings show that plants use H3K4me3 demethylase to constitutively remove active chromatin mark and maintain silencing status at a subset retrotransposons which localize in heterochromatin regions. Therefore, our work uncovers a novel mechanism to control retrotransposon activity by histone demethylation, which further strengthens the link between epigenetic silencing and genome stability. Examination of differences in H3K4 between jmj703 and wild type.
2013-01-01 | E-GEOD-41183 | biostudies-arrayexpress
Project description:Heterochromatin constitutes a fundamental aspect of genomes that is crucial for maintaining genome stability. In flowering plants, maintenance of heterochromatin relies on a positive feedback loop involving the histone 3 lysine nine methyltransferase (H3K9), KRYPTONITE (KYP), and the DNA methyltransferase, CHROMOMETHYLASE3 (CMT3). An H3K9 demethylase, INCREASED IN BONSAI METHYLATION 1 (IBM1), has evolved to modulate the activity of KYP-CMT3 within transcribed genes. The absence of IBM1 activity results in aberrant methylation of gene bodies, which is deleterious. This study demonstrates extensive genetic and gene expression variations in KYP, CMT3, and IBM1 within and between flowering plant species. IBM1 activity in Arabidopsis thaliana is uniquely regulated by the abundance of H3K9me2 in a repetitive sequence within an intron preceding the histone demethylase domain. This mechanism enables IBM1 to monitor global levels of H3K9me2. We discovered that the methylated intron is prevalent across flowering plants, however, its underlying sequence exhibits dynamic evolution. Its absence in species lacking gene body DNA methylation suggests its primary role in sensing H3K9me2 and preventing its integration into these constitutively expressed genes. Furthermore, our investigation uncovered Arabidopsis thaliana accessions resembling weak ibm1 mutants, several Brassicaceae species with reduced IBM1 expression, and a potential IBM1 deletion. Evolution towards reduced IBM1 activity in some flowering plants could explain the frequent natural occurrence of diminished or lost CMT3 activity, as cmt3 mutants in A. thaliana mitigate the deleterious effects of IBM1.
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Project description:Histone methylation plays important roles in the regulation of chromatin dynamics and transcription. Steady state levels of histone lysine methylation are regulated by a balance between enzymes that catalyze either the addition or removal of methyl groups. Using an activity-based biochemical approach, we recently uncovered the JmjC domain as an evolutionarily conserved signature motif for histone demethylases. Furthermore, we demonstrated that Jhd1, a JmjC domain-containing protein in S. cerevisiae, is an H3K36-specific demethylase. Here we report further characterization of Jhd1. Similar to its mammalian homolog, Jhd1-catalyzed histone demethylation requires iron and alpha-ketoglutarate as cofactors. Mutation and deletion studies indicate that the JmjC domain and adjacent sequences are critical for Jhd1 enzymatic activity, while the N-terminal PHD domain is dispensable. Overexpression of JHD1 results in a global reduction of H3K36 methylation in vivo. Finally, chromatin immunoprecipitation coupled microarray (ChIP-chip) studies reveal subtle changes in the distribution of H3K36me2 upon overexpression or deletion of JHD1. Our studies establish Jhd1 as a histone demethylase in budding yeast and suggest that Jhd1 functions to maintain the fidelity of histone methylation patterns along transcription units. Keywords: ChIP-chip
2007-05-04 | GSE7627 | GEO
Project description:In diverse eukaryotes, constitutively silent sequences, such as transposons and repeats, are marked by methylation at histone H3 lysine 9 (H3K9me). Despites the conservation and importance in the genome integrity, mechanisms to exclude H3K9m from active genes remained largely unexplored. Here we show in Arabidopsis that the exclusion depends on a histone demethylase gene, IBM1 (increase in BONSAI methylation); loss-of-function ibm1 mutation caused ectopic H3K9me in thousands of genes, which accompanies genic DNA methylation at non-CG sites. The ibm1-induced genic H3K9me depended on both histone methylase KYP/SUVH4 and DNA methylase CMT3, suggesting interdependence of two epigenetic marks – H3K9me and non-CG methylation. Notably, IBM1 enhanced loss of H3K9m in transcriptionally de-repressed sequences. Furthermore, disruption of transcription in genes induced ectopic non-CG methylation, mimicking the loss of IBM1 function. We propose that active chromatin is stabilized by the autocatalytic loop of transcription and H3K9 demethylation. This process counteracts accumulation of silent epigenetic marks, H3K9me and non-CG methylation, which is also autocatalytic.
2010-09-21 | GSE22953 | GEO