Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and ibm1-3 trancriptomes in normal light and high light condition

ABSTRACT: 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

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE106568 | GEO | 2018/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide analysis of H3K9me2 in ibm1, kyp, and cmt3 mutants of Arabidopsis thaliana

2010-09-21 | GSE22953 | GEO

Dysfunction of histone demethylase IBM1 in Arabidopsis causes autoimmunity and reshapes the root microbiome

Project description:Root microbiota is important for plant growth and fitness. Little is known about whether and how the assembly of root microbiota may be controlled by epigenetic regulation, which is crucial for gene transcription and genome stability. Here we show that dysfunction of the histone demethylase IBM1 (INCREASE IN BONSAI METHYLATION 1) in Arabidopsis thaliana substantially reshaped the root microbiota, with the majority of the significant amplicon sequence variants (ASVs) being decreased. Transcriptome analyses of plants grown in soil and in sterile growth-medium jointly disclosed salicylic acid (SA)-mediated autoimmunity and production of the defense metabolite camalexin in the ibm1 mutants. Analyses of genome-wide histone modifications and DNA methylation highlighted epigenetic modifications permissive for transcription at several important defense regulators. Consistently, ibm1 mutants showed increased resistance to the pathogen Pseudomonas syringae DC3000 with stronger immune responses. In addition, ibm1 showed substantially impaired plant growth-promotion in response to beneficial bacteria; the impairment was partially mimicked by exogenous application of SA to wild type plants, and by a null mutation of AGP19 that is important for cell expansion and that is repressed with DNA hyper methylation in ibm1. IBM1-dependent epigenetic regulation imposes strong and broad impacts on plant-microbe interactions and thereby shapes the assembly of root microbiota.

2022-07-28 | GSE173239 | GEO

IBM1, a JmjC domain histone demethylase, is involved in the regulation of RNA-directed DNA methylation through epigenetic control of RDR2 and DCL3 expression in Arabidopsis.

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

IBM1, a JmjC domain histone demethylase, is involved in the regulation of RNA-directed DNA methylation through epigenetic control of RDR2 and DCL3 expression in Arabidopsis.

2012-08-03 | GSE32284 | GEO

Genome-wide analysis of H3K9me2 in ibm1, kyp, and cmt3 mutants of Arabidopsis thaliana

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. Leaves of 4-week-old plants were fixed as described previously (Saze et al, 2008). Chromatin immunoprecipitation (ChIP) was performed as described previously (Kimura et al, 2008), using antibody against H3K9me2 (CMA307, Kimura et al, 2008, PMID: 18227620). Non-immunoprecipitated DNA (input DNA) and ChIP samples were amplified, labeled, and hybridized to microarray according to the manufacturer’s instruction (Protocols for Chromatin Immunoprecipitation and Amplification, NimbleGen). Input DNA and ChIP DNA were differentially labeled with Cy3 and Cy5, respectively, and competitively hybridized to a microarray chip. We used NimbleGen 2.1M HD2 array covering entire genome of A. thaliana.

2010-09-21 | E-GEOD-22953 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:Epigenetic regulation of light-induced anthocyanin biosynthesis by IBM1 histone demethylase in Arabidopsis

| PRJNA415344 | ENA

Transcriptome analysis of apple peel samples at different time points in the process of changing from green to red under light conditions after unbagging

Project description:Purpose:The red coloration of apple (Malus × domestica Borkh.) is due to the accumulation of anthocyanins in the fruit peel. Light is essential for anthocyanin biosynthesis in apple.Apple peel can quickly turn red under light conditions after unbagging. Therefore, the implementation of transcriptome sequencing to find genes that promote anthocyanin accumulation in response to light signals is necessary to clarify the mechanism of light-induced anthocyanin accumulation in apple peel.

2021-10-02 | GSE185089 | GEO

Expression data of Arabidopsis thaliana (Ler accession) phytochrome phyABCDE quintuple mutant and phyABDE quadruple mutant in response to red light, and their comparison to WT expression data

Project description:Phytochromes are red/far-red light photoreceptors. We sought to test at the transcriptomic level if Arabidopsis mutants lacking all phytochromes (from phyA to phyE), or just retaining trace levels of phyC, had transcriptional response to red light exposure.

2012-04-01 | GSE31587 | GEO

MethlyC-Seq of ibm1-4

Project description:Using MethylC-Seq to provide single-base resulution of DNA methylation status in ibm1-4 mutant 1 sample examined, ibm1-4 mutant

2013-09-06 | E-GEOD-48053 | biostudies-arrayexpress

Phytochrome Interacting Factors 4 and 5 redundantly limit seedling de-etiolation in continuous far-red light.

Project description:Phytochromes are red/far red photosensors regulating numerous developmental programs in plants. Among them phytochrome A (phyA) is essential to enable seedling de-etiolation in continuous far-red (FR) light a condition mimicking the environment under a dense canopy. The ecological relevance of this response is demonstrated by the high mortality rate of phyA mutants germinating in deep vegetational shade. phyA signaling involves a direct interaction of the photoreceptor with members of the bHLH transcription factor family, PIF1 and PIF3 (Phytochrome Interacting Factor). Here we investigated the involvement of PIF4 and PIF5 in phyA signaling and found that they redundantly control de-etiolation in FR light. The pif4pif5 double mutant is hypersensitive to low fluence rates of FR light. This phenotype is dependent on FR light perception by phyA but does not rely on alterations of the phyA level. Our microarrays analysis shows that PIF4 and PIF5 are part of an inhibitory mechanism repressing the expression of some light-responsive genes in the dark and are also needed for full expression of several growth-related genes in the light. Unlike PIF1 and PIF3, PIF4 and PIF5 are not degraded in response to FR light indicating that they are light-regulated by a different mechanism. Our genetic analysis suggests that this is achieved through the sequestration of these PIFs by the closely related bHLH transcription factor HFR1 (long Hypocotyl in FR light).

2009-08-19 | GSE16333 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data