Dissecting the Dynamic Changes of Methylome and Transcriptome During Rice Transformation
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa
PROVIDER: GSE202715 | GEO | 2023/09/27
REPOSITORIES: GEO
Similar Datasets
Project description:Transposable elements (TEs) and repetitive sequences comprise over 40% of rice genome. Different TEs are tightly regulated by distinct epigenetic mechanisms. For example, the activities of LTR retrotransposon Tos17 and non-LTR retrotransposon LINE element Karma are uniquely regulated by histone H3K9 methylation and histone H3K4 demethylation, respectively. Miniature inverted repeat transposable elements (MITEs) are one of the most high-copy-number DNA transposons, which are interspersed around rice genome and might influence nearby gene expression. In plants, 24-nucleotide (24-nt) heterochromatic small interfering RNAs (hc-siRNAs) derived from repeats and TEs. To what extent hc-siRNA associated TEs affect gene expression and therefore contribute to agricultural traits in rice remains elusive. Here, we show that OsDCL3a, one of Dicer-Like 3 (DCL3) homolog, is primarily responsible for 24-nt hc-siRNA processing in rice. Impaired OsDCL3a displayed altered important agricultural traits in rice. We found that genome-wide (281,563) 24-nt hc-siRNA clusters were OsDCL3a-dependent, among which MITEs were significantly enriched. Impaired OsDCL3a caused significant overlapping between reduced hc-siRNAs from MITEs and elevated nearby gene expression. Intriguingly, genes involved in Gibberellin and Brassinosteroid homeostasis were identified as direct targets of OsDCL3a, which may attribute to dwarfism and enlarged flag leaf angle upon OsDCL3a deficiency. Our work uncovers OsDCL3a-dependent hc-siRNAs derived from MITEs as broad spectrum of regulators for fine-tuning gene expression, and this observation may reflect a conserved mechanism in other higher plants with dispersed repeat- or TE-rich genomes. Examination of OsDCL3a-dependent hc-siRNAs derived from MITEs.
2014-02-04 | E-GEOD-50778 | biostudies-arrayexpress
Project description:Twenty-four nucleotide long miRNAs (lmiRNAs) direct DNA methylation at target genes and regulate their transcription. The evolutionary origin of lmiRNAs and the range of lmiRNA-mediated regulation remain obscure. Here, we reannotated lmiRNAs and their targets in rice by applying stringent criteria. We found that the majority of lmiRNAs are derived from MITEs and most sites targeted by MITE-derived lmiRNAs reside within MITEs, suggesting co-evolution of lmiRNAs and their targets through MITE amplification. lmiRNAs undergo dynamically changes under stressed conditions and the genes targeted by lmiRNAs show an enrichment for stress responsive genes, suggesting that lmiRNAs are widely involved in plant response to stresses. We constructed the evolutionary histories of lmiRNAs and their targets. lmiRNAs emerged before or when the AA genome was diverged, while the emergence of lmiRNA targets coincided with or followed the emergence of lmiRNAs. Furthermore, we found that the sequences of a lmiRNA target site underwent variations, coincident with the divergence of rice accessions and the distribution of rice accessions in different geographical locations and climatic conditions. Our findings highlight MITEs as an important origin of lmiRNAs and suggest that the evolution of lmiRNA-target regulatory modules may contribute to rice adaptation to environmental changes.
2023-11-01 | GSE217602 | GEO
Project description:Transposable elements (TEs) and repetitive sequences comprise over 40% of rice genome. Different TEs are tightly regulated by distinct epigenetic mechanisms. For example, the activities of LTR retrotransposon Tos17 and non-LTR retrotransposon LINE element Karma are uniquely regulated by histone H3K9 methylation and histone H3K4 demethylation, respectively. Miniature inverted repeat transposable elements (MITEs) are one of the most high-copy-number DNA transposons, which are interspersed around rice genome and might influence nearby gene expression. In plants, 24-nucleotide (24-nt) heterochromatic small interfering RNAs (hc-siRNAs) derived from repeats and TEs. To what extent hc-siRNA associated TEs affect gene expression and therefore contribute to agricultural traits in rice remains elusive. Here, we show that OsDCL3a, one of Dicer-Like 3 (DCL3) homolog, is primarily responsible for 24-nt hc-siRNA processing in rice. Impaired OsDCL3a displayed altered important agricultural traits in rice. We found that genome-wide (281,563) 24-nt hc-siRNA clusters were OsDCL3a-dependent, among which MITEs were significantly enriched. Impaired OsDCL3a caused significant overlapping between reduced hc-siRNAs from MITEs and elevated nearby gene expression. Intriguingly, genes involved in Gibberellin and Brassinosteroid homeostasis were identified as direct targets of OsDCL3a, which may attribute to dwarfism and enlarged flag leaf angle upon OsDCL3a deficiency. Our work uncovers OsDCL3a-dependent hc-siRNAs derived from MITEs as broad spectrum of regulators for fine-tuning gene expression, and this observation may reflect a conserved mechanism in other higher plants with dispersed repeat- or TE-rich genomes.
2014-02-04 | GSE50778 | GEO
Project description:Most transgenic crops are produced through tissue culture. The impact of utilizing such methods on the plant epigenome is poorly understood. Here we generated whole-genome, single-nucleotide resolution maps of DNA methylation in several transgenic rice lines. We found that all tested transgenic plants had significant losses of methylation compared to untransformed plants. Loss of methylation was largely stable across generations, and certain sites in the genome were particularly susceptible to loss of methylation. Loss of methylation at promoters was associated with deregulated expression of protein-coding genes. Analyses of callus and untransformed plants regenerated from callus indicated that loss of methylation is stochastically induced at the tissue culture step. These changes in methylation may explain a component of somaclonal variation, a phenomenon in which plants derived from tissue culture manifest phenotypic variability. Whole genome methylation maps of rice were generated using BS-seq (Hume Stroud, Suhua Feng, Steve Jacobsen at UCLA). Whole genome expression maps of rice were generated using mRNA-seq and smRNA (Stacey Simon, Blake Meyers at Univ of Delaware).
2013-03-26 | E-GEOD-42410 | biostudies-arrayexpress
Project description:In rice, tillering is an important agricultural trait that affects plant architecture and grain yield. RNA-directed DNA methylation (RdDM), which establishes DNA methylation in all CG, CHG and CHH sequence contexts and maintains CHH methylation in plants, silences transposable elements (TEs) and regulates gene expression. Here we report that knockdown and knockout of OsNRPD1a and OsNRPD1b, genes encoding two orthologues of the largest subunit of OsPol IV holoenzyme that transcribes 24-nucleotide (nt) siRNAs in RdDM, lead to a high-tillering phenotype, in addition to dwarfism and smaller panicles. In the shoot base of the osnrpd1a/b RNAi line, many genes are dysregulated, due to loss of 24-nt siRNAs and CHH methylation. Among these genes, OsMIR156d and OsMIR156j, which promote rice tillering, is derepressed when CHH methylation at Miniature Inverted-Repeat Transposable Elements (MITEs) in the promoters of OsMIR156d and OsMIR156j is lost. By contrast, D14, which suppresses rice tillering, is repressed when CHH methylation at a MITE in the 3’UTR of D14 is lost. Deletion of the MITE that is targeted by RdDM in D14 is sufficient to cause high-tillering. Our findings reveal control of rice tillering by RdDM at MITEs and provide the potential targets for agronomic trait enhancement by epigenome editing.
2020-03-16 | GSE131319 | GEO
Project description:The oil palm fruit abnormality, mantled, is a somaclonal variant arising from tissue culture that drastically reduces yield, and has largely halted efforts to clone elite hybrids for breeding and oil production. Widely regarded as epigenetic, mantling had defied explanation, and has become an icon of unsustainability in environmentally sensitive tropical plantation crops. We identified the MANTLED gene using Epigenome Wide Association analysis of genetically identical palms from multiple clonal lineages. Hypomethylation of a LINE retrotransposon related to rice Karma, found in the intron of the homeotic gene DEFICIENS, is common to all mantled clones and is correlated with alternative splicing and loss of small RNA. DNA methylation is regained in spontaneous revertants accounting for non-Medelian inheritance of the Good Karma and Bad Karma epialleles. Thus epigenetic regulation of transposable elements results in somaclonal variation and provides a means to cull mantled nursery palms before committing limiting plantation resources to clonal propagation. DNA methylation profiling was performed using the McrBC DNA methylation dependent fractionation and microarray hybridization method as described in Lippman, Z., Gendrel, A. V., Colot, V. & Martienssen, R. Profiling DNA methylation patterns using genomic tiling microarrays. Nat Methods 2, 219-224 (2005).
2015-09-09 | GSE68410 | GEO
Project description:The oil palm fruit abnormality, mantled, is a somaclonal variant arising from tissue culture that drastically reduces yield, and has largely halted efforts to clone elite hybrids for breeding and oil production. Widely regarded as epigenetic, mantling had defied explanation, and has become an icon of unsustainability in environmentally sensitive tropical plantation crops. We identified the MANTLED gene using Epigenome Wide Association analysis of genetically identical palms from multiple clonal lineages. Hypomethylation of a LINE retrotransposon related to rice Karma, found in the intron of the homeotic gene DEFICIENS, is common to all mantled clones and is correlated with alternative splicing and loss of small RNA. DNA methylation is regained in spontaneous revertants accounting for non-Medelian inheritance of the Good Karma and Bad Karma epialleles. Thus epigenetic regulation of transposable elements results in somaclonal variation and provides a means to cull mantled nursery palms before committing limiting plantation resources to clonal propagation. DNA methylation profiling was performed using the McrBC DNA methylation dependent fractionation and microarray hybridization method as described in Lippman, Z., Gendrel, A. V., Colot, V. & Martienssen, R. Profiling DNA methylation patterns using genomic tiling microarrays. Nat Methods 2, 219-224 (2005). DNA methylation profiling was performed on 54 parthenocarpic mantled ramet, 43 normal ramet and 1 ortet adult leaf samples. For each sample, two independent fractionations of total genomic DNA and DNA methylation-depleted DNA were performed. Each total DNA/methylation-depleted DNA pair was differentially labeled and hydrized to a custon Nimblegen microarray in a dye-swapped design (4 array hybridizations per sample).
2015-09-09 | E-GEOD-68410 | biostudies-arrayexpress
Project description:Most transgenic crops are produced through tissue culture. The impact of utilizing such methods on the plant epigenome is poorly understood. Here we generated whole-genome, single-nucleotide resolution maps of DNA methylation in several transgenic rice lines. We found that all tested transgenic plants had significant losses of methylation compared to untransformed plants. Loss of methylation was largely stable across generations, and certain sites in the genome were particularly susceptible to loss of methylation. Loss of methylation at promoters was associated with deregulated expression of protein-coding genes. Analyses of callus and untransformed plants regenerated from callus indicated that loss of methylation is stochastically induced at the tissue culture step. These changes in methylation may explain a component of somaclonal variation, a phenomenon in which plants derived from tissue culture manifest phenotypic variability.
2013-03-26 | GSE42410 | GEO
Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling
network (bRaf mutated)
Crosstalk model of the ERK, Wnt and Akt
signalling pathways with bRaf mutation
This model is described in the article:
Cancerous perturbations
within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network
constitutively activate inter-pathway positive feedback
loops.
Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
Mol Biosyst 2017 May; 13(5):
830-840
Abstract:
Perturbations in molecular signaling pathways are a result
of genetic or epigenetic alterations, which may lead to
malignant transformation of cells. Despite cellular robustness,
specific genetic or epigenetic changes of any gene can trigger
a cascade of failures, which result in the malfunctioning of
cell signaling pathways and lead to cancer phenotypes. The
extent of cellular robustness has a link with the architecture
of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000653.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000653 | BioModels
Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling
network (EGFR overexpression)
Crosstalk model of the ERK, Wnt and Akt
signalling pathways with EGFR overexpression.
This model is described in the article:
Cancerous perturbations
within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network
constitutively activate inter-pathway positive feedback
loops.
Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
Mol Biosyst 2017 May; 13(5):
830-840
Abstract:
Perturbations in molecular signaling pathways are a result
of genetic or epigenetic alterations, which may lead to
malignant transformation of cells. Despite cellular robustness,
specific genetic or epigenetic changes of any gene can trigger
a cascade of failures, which result in the malfunctioning of
cell signaling pathways and lead to cancer phenotypes. The
extent of cellular robustness has a link with the architecture
of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000656.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000656 | BioModels