Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE106157
PROVIDER: PRJNA417159 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Paternal chromosome loss and metabolic crisis contribute to hybrid inviability in Xenopus
| PRJNA415788 | ENA
Project description:Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which characterizes many silenced genes including those on the inactive X-chromosome. Here we interrogate the role of core PRC2 protein EED in X-linked gene silencing by assessing allele-specific X-linked gene expression in WT and Eed-/- hybrid mouse trophoblast stem cells (TSCs) harboring a 129/S1-derived maternal X-chromosome and a JF1/Ms-derived paternal X-chromosome. This study generates mRNA-seq data for WT and Eed-/- TSCs, which undergo imprinted inactivation of the paternal X-chromosome. RNA-seq data was mapped allele-specifically to in silico strain-specific maternal and paternal reference genomes, generated based on known single nucleotide polymorphisms. We find that EED loss abrogates H3K27me3 and expression of Xist lncRNA, which is required for X-inactivation, however, despite the absence of H3K27me3 and Xist, only a subset of PRC2 target genes are derepressed in Eed-/- TSCs.
2017-04-07 | GSE84681 | GEO
Project description:Development of the early embryo is thought to be mainly driven by maternal gene products and post-transcriptional gene regulation. Here, we used metabolic labeling to show that RNA can be transferred by sperm into the embryo. To identify genes with paternal expression in the embryo, we performed crosses of males and females from divergent C. elegans strains. RNA sequencing of mRNAs and small RNAs in the 1-cell hybrid embryo revealed that about two hundred paternal mRNAs are reproducibly expressed in the embryo, and that about half of assayed endogenous siRNAs and piRNAs are also of paternal origin. Together, our results suggest an unexplored paternal contribution to early development. To reveal the identity of paternal RNA molecules, we performed a cross of males and females from two divergent C. elegans strains because we reasoned that sequencing of embryonic RNA and SNP analysis should then identify and quantify maternal and paternal transcripts. These sequencing experiments were carried out in purified hybrid 1-cell embryos and comprised small RNAs and mRNAs. For comparison we sequenced mRNAs and small RNAs from the parental strains: paternal (Hawaiian males, CB4856) and maternal (fem-1(hc17ts)/TX189(OMA-1::GFP). For the annotation of strain specific mutations (SNPs) we sequenced mRNA and small RNAs extracted from whole worms. All experiments were performed in at least two independent biological replicates.
2014-06-04 | E-GEOD-57351 | biostudies-arrayexpress
Project description:KDM6A, which regulates gene expression by demethylation of the repressive histone mark H3K27me3, has a higher level in mammalian females than in males because the Kdm6a gene escapes X chromosome inactivation. Here, we report that maternal and paternal alleles of a number of genes throughout the genome are differentially regulated by KDM6A. Knockout of KDM6A in male and female embryonic stem cells derived from F1 hybrid mice results in downregulation of maternal alleles more frequently than paternal alleles. This parent-of-origin preference for regulation of gene expression by KDM6A was observed for subsets of maternally expressed non-imprinted and imprinted genes. By ATAC-seq downregulated genes showed a concomitant loss of chromatin accessibility on maternal but not on paternal alleles. Surprisingly, enrichment in H3K27me3 was observed on downregulated paternal but not maternal alleles. These results suggest parent-of-origin mechanisms of gene regulation by KDM6A, which may be histone demethylation-dependent and -independent.
2022-07-26 | GSE209788 | GEO
Project description:KDM6A, which regulates gene expression by demethylation of the repressive histone mark H3K27me3, has a higher level in mammalian females than in males because the Kdm6a gene escapes X chromosome inactivation. Here, we report that maternal and paternal alleles of a number of genes throughout the genome are differentially regulated by KDM6A. Knockout of KDM6A in male and female embryonic stem cells derived from F1 hybrid mice results in downregulation of maternal alleles more frequently than paternal alleles. This parent-of-origin preference for regulation of gene expression by KDM6A was observed for subsets of maternally expressed non-imprinted and imprinted genes. By ATAC-seq downregulated genes showed a concomitant loss of chromatin accessibility on maternal but not on paternal alleles. Surprisingly, enrichment in H3K27me3 was observed on downregulated paternal but not maternal alleles. These results suggest parent-of-origin mechanisms of gene regulation by KDM6A, which may be histone demethylation-dependent and -independent.
2022-07-26 | GSE209787 | GEO
Project description:KDM6A, which regulates gene expression by demethylation of the repressive histone mark H3K27me3, has a higher level in mammalian females than in males because the Kdm6a gene escapes X chromosome inactivation. Here, we report that maternal and paternal alleles of a number of genes throughout the genome are differentially regulated by KDM6A. Knockout of KDM6A in male and female embryonic stem cells derived from F1 hybrid mice results in downregulation of maternal alleles more frequently than paternal alleles. This parent-of-origin preference for regulation of gene expression by KDM6A was observed for subsets of maternally expressed non-imprinted and imprinted genes. By ATAC-seq downregulated genes showed a concomitant loss of chromatin accessibility on maternal but not on paternal alleles. Surprisingly, enrichment in H3K27me3 was observed on downregulated paternal but not maternal alleles. These results suggest parent-of-origin mechanisms of gene regulation by KDM6A, which may be histone demethylation-dependent and -independent.
2022-07-26 | GSE209786 | GEO
Project description:Interspecific hybridization often induces epigenetic remodeling that leads to transposon activation, gene expression changes, and loss of imprinting. These genomic changes can be deleterious and lead to postzygotic hybrid incompatibility. In Arabidopsis, loss of genomic imprinting of PHERES1 and presumed failure of Polycomb Repressive Complex is partially responsible for seed inviability observed in A. thaliana X A. arenosa interspecific hybrids. We used this species pair to further analyze the relationship between parent-specific gene expression and postzygotic hybrid incompatibility using two A. thaliana ecotypes, Col-0 and C24, with differential seed survival. We found that maternal imprinting was perturbed for PHERES1, HDG3, and six other genes in both A. thaliana hybrids and paternal imprinting was lost for MEDEA as observed previously. Three classes of retroelements; Sadhu, Athila, and Copia, maintained proper repression patterns suggesting some regulatory mechanisms are not disrupted early in development. We propose that early genome remodeling and loss of imprinting of seed development genes induces lethality in both compatible and incompatible hybrids. We examined gene expression in A. thaliana intraspecific hybrid crosses to determine normal patterns of maternal and paternal expression early in seed development.
2015-03-02 | E-GEOD-56675 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE9504: Expression data from hybrid female Xenopus sex reversal experiment; GSE9505: Expression data from hybrid male Xenopus sex reversal experiment Experiment Overall Design: Refer to individual Series
2008-06-16 | E-GEOD-9507 | biostudies-arrayexpress
Project description:Development of the early embryo is thought to be mainly driven by maternal gene products and post-transcriptional gene regulation. Here, we used metabolic labeling to show that RNA can be transferred by sperm into the embryo. To identify genes with paternal expression in the embryo, we performed crosses of males and females from divergent C. elegans strains. RNA sequencing of mRNAs and small RNAs in the 1-cell hybrid embryo revealed that about two hundred paternal mRNAs are reproducibly expressed in the embryo, and that about half of assayed endogenous siRNAs and piRNAs are also of paternal origin. Together, our results suggest an unexplored paternal contribution to early development.
2014-06-04 | GSE57351 | GEO
Project description:Hybrid phenotypes that contribute to postzygotic reproductive isolation often exhibit pronounced asymmetry, both between reciprocal crosses and between the sexes in accordance with Haldane's rule. Inviability in mammalian hybrids is associated with parent-of-origin placental growth abnormalities for which misregulation of imprinted genes is the leading candidate mechanism. However, direct evidence for the involvement of imprinted genes in hybrid growth dysplasia is limited. We used transcriptome and reduced representation bisulfite sequencing to conduct the first genome-scale assessment of the contribution of imprinted genes to parent-of-origin placental growth dysplasia in the cross between the house mouse (Mus musculus domesticus) and the Algerian mouse (Mus spretus). Imprinted genes with transgressive expression and methylation were concentrated in the Kcnq1 cluster, which contains causal genes for prenatal growth abnormalities in mice and humans. Hypermethylation of the cluster’s imprinting control region, and consequent misexpression of the genes Phlda2 and Ascl2, is a strong candidate mechanism for transgressive placental undergrowth. Transgressive placental and gene regulatory phenotypes, including expression and methylation in the Kcnq1 cluster, were more extreme in hybrid males. While consistent with Haldane’s rule, male-biased defects are unexpected in rodent placenta because the X-chromosome is effectively hemizygous in both sexes. In search of an explanation we found evidence of leaky imprinted (paternal) X-chromosome inactivation in hybrid female placenta, an epigenetic disturbance that may buffer females from the effects of X-linked incompatibilities to which males are fully exposed. Sex differences in chromatin structure on the X and sex-biased maternal effects are non-mutually exclusive alternative explanations for adherence to Haldane’s rule in hybrid placenta. The results of this study contribute to understanding the genetic basis of hybrid inviability in mammals, and the role of imprinted genes in speciation.
2020-11-09 | GSE161051 | GEO