A small RNA pathway mediates allelic dosage in endosperm
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ABSTRACT:
PROVIDER: PRJNA374335 | ENA |
REPOSITORIES: ENA
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Project description:A small RNA pathway mediates allelic dosage in endosperm [sRNA-seq]
| PRJNA374333 | ENA
Project description:Balance between maternal and paternal genomes within the triploid endosperm is necessary for normal seed development. The majority of endosperm genes are expressed in a 2:1 maternal:paternal ratio, reflecting genomic DNA content. Here we find that the 2:1 transcriptional ratio is, unexpectedly, actively regulated. In A. thaliana and A. lyrata, endosperm 24 nt small RNAs are reduced in TEs and enriched in genes compared to the embryo. We find an inverse relationship between the parent-of-origin of sRNAs and mRNAs, with genes more likely to be associated with maternally than paternally biased sRNAs. Disruption of the Pol IV sRNA pathway causes a shift toward maternal allele mRNA expression for many genes. Furthermore, paternal inheritance of an RNA Pol IV mutation is sufficient to rescue seed abortion caused by excess paternal genome dosage. Thus, RNA Pol IV mediates transcriptional balance between maternally and paternally inherited genomes in endosperm.
2017-12-15 | GSE94787 | GEO
Project description:Balance between maternal and paternal genomes within the triploid endosperm is necessary for normal seed development. The majority of endosperm genes are expressed in a 2:1 maternal:paternal ratio, reflecting genomic DNA content. Here we find that the 2:1 transcriptional ratio is, unexpectedly, actively regulated. In A. thaliana and A. lyrata, endosperm 24 nt small RNAs are reduced in TEs and enriched in genes compared to the embryo. We find an inverse relationship between the parent-of-origin of sRNAs and mRNAs, with genes more likely to be associated with maternally than paternally biased sRNAs. Disruption of the Pol IV sRNA pathway causes a shift toward maternal allele mRNA expression for many genes. Furthermore, paternal inheritance of an RNA Pol IV mutation is sufficient to rescue seed abortion caused by excess paternal genome dosage. Thus, RNA Pol IV mediates transcriptional balance between maternally and paternally inherited genomes in endosperm.
2017-12-15 | GSE94786 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-12-15 | GSE94792 | GEO
Project description:Seed development is sensitive to parental dosage, with excess maternal or paternal genomes creating reciprocal phenotypes. Paternal genomic excess results in extensive endosperm proliferation without cellularization and eventual seed abortion. We previously showed that loss of the RNA POL IV gene nrpd1 in tetraploid fathers represses seed abortion in paternal excess crosses. Here we show genetically that RNA-directed DNA methylation (RdDM) pathway activity in the paternal parent is sufficient to determine the viability of paternal excess seeds. The status of the RdDM pathway in paternal excess endosperm does not impact seed viability. Comparison of endosperm transcriptomes, DNA methylation, and small RNAs from balanced and paternal excess endosperm demonstrates that paternal excess seed abortion is unlikely to be dependent on either transposable element or imprinted gene mis-regulation. We suggest instead that loss of paternal RdDM modulates expression at a small subset of genes and desensitizes endosperm to paternal excess. Finally, using allele-specific transcription data, we present evidence of a transcriptional buffering system that up37 regulates maternal alleles and represses paternal alleles in response to excess paternal genomic dosage. These findings prompt reconsideration of models for dosage sensitivity in endosperm.
2019-05-01 | GSE126931 | GEO
Project description:Seed development is sensitive to parental dosage, with excess maternal or paternal genomes creating reciprocal phenotypes. Paternal genomic excess results in extensive endosperm proliferation without cellularization and eventual seed abortion. We previously showed that loss of the RNA POL IV gene nrpd1 in tetraploid fathers represses seed abortion in paternal excess crosses. Here we show genetically that RNA-directed DNA methylation (RdDM) pathway activity in the paternal parent is sufficient to determine the viability of paternal excess seeds. The status of the RdDM pathway in paternal excess endosperm does not impact seed viability. Comparison of endosperm transcriptomes, DNA methylation, and small RNAs from balanced and paternal excess endosperm demonstrates that paternal excess seed abortion is unlikely to be dependent on either transposable element or imprinted gene mis-regulation. We suggest instead that loss of paternal RdDM modulates expression at a small subset of genes and desensitizes endosperm to paternal excess. Finally, using allele-specific transcription data, we present evidence of a transcriptional buffering system that up37 regulates maternal alleles and represses paternal alleles in response to excess paternal genomic dosage. These findings prompt reconsideration of models for dosage sensitivity in endosperm.
2019-05-01 | GSE126930 | GEO
Project description:Seed development is sensitive to parental dosage, with excess maternal or paternal genomes creating reciprocal phenotypes. Paternal genomic excess results in extensive endosperm proliferation without cellularization and eventual seed abortion. We previously showed that loss of the RNA POL IV gene nrpd1 in tetraploid fathers represses seed abortion in paternal excess crosses. Here we show genetically that RNA-directed DNA methylation (RdDM) pathway activity in the paternal parent is sufficient to determine the viability of paternal excess seeds. The status of the RdDM pathway in paternal excess endosperm does not impact seed viability. Comparison of endosperm transcriptomes, DNA methylation, and small RNAs from balanced and paternal excess endosperm demonstrates that paternal excess seed abortion is unlikely to be dependent on either transposable element or imprinted gene mis-regulation. We suggest instead that loss of paternal RdDM modulates expression at a small subset of genes and desensitizes endosperm to paternal excess. Finally, using allele-specific transcription data, we present evidence of a transcriptional buffering system that up37 regulates maternal alleles and represses paternal alleles in response to excess paternal genomic dosage. These findings prompt reconsideration of models for dosage sensitivity in endosperm.
2019-05-01 | GSE126929 | GEO
Project description:A small RNA pathway mediates allelic dosage in endosperm [mRNA-seq]
| PRJNA374044 | ENA
Project description:Paternally-acting canonical RNA-directed DNA methylation pathway genes sensitizes Arabidopsis endosperm to paternal dosage
| PRJNA523797 | ENA
Project description:Biallelic expression is important to ensure adequate mRNA levels as well as protect cells from deleterious heterozygous mutations. However, the factors determining biallelic expression at individual gene loci are unknown. Deletion of the MSL complex component MSL2 in hybrid mouse NPCs uncovers an unprecedented function for MSL2 in allelic regulation. While biallelically expressed in wildtype NPCs, a class of MSL2 targets switches from bi to monoallelic expression upon MSL2 loss. The silenced allele loses nascent transcription, accompanied by dramatic changes in local chromatin landscape such as monoallelic gain of H3K27me3 and DNA methylation. Meanwhile, active histone modifications, RNA POL II, BRD4 and KANSL3 are retained on the active allele. MSL2 targets include several sex-biased genes on autosomes as well as X-chromosomal genes that escape X inactivation. Together, the allele-specific resolution allowed us to unravel an MSL2 mediated safeguarding mechanism to promote biallelic gene expression of sexually dimorphic and dosage-sensitive genes in mammals.
2023-08-10 | GSE183766 | GEO