Arabidopsis thaliana x Arabidopsis arenosa
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ABSTRACT:
PROVIDER: PRJNA176730 | ENA |
REPOSITORIES: ENA
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Project description:Interspecific hybrids in Arabidopsis result in seed abortion that causes reproductive barrier. To investigate the allelic expression pattern at transcriptome level during early seed abortion stage, we performed RNA-seq analysis in F1 interspecific hybrids with three different ecotypes in A. thaliana as maternal and A. arenosa as paternal and identified MEGs and PEGs. Interestingly, PEGs showed distinct expression pattern in several aspects, compared to MEGs: PEGs showed ecotype-specific expression pattern, suggesting a role for PEGs in ecotype-dependent seed lethality. 35% of previously known MEGs in non-lethal hybrids were found as PEGs in our lethal interspecific hybrids, implying the presence of abnormal paternal allelic upregulation. The correlation test between the upregulation of PEGs and previously reported paternal-excess interploidy cross (2X6) which exhibited seed abortion showed that dosage disruption by abnormal paternal upregulation is correlated with seed abortion. Moreover, epigenetic disruption appears to cause some of abnormal upregulation of paternal alleles in PEGs via mis-regulation of MEA-mediated PcG2 and MET1-mediated DNA methylation. The results provide clue on the critical role of PEGs in seed abortion via disruption of dosage balance and epigenetic regulation.
2015-10-01 | GSE41391 | 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: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.
2015-03-02 | GSE56675 | 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: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:The "triploid block" prevents interploidy hybridizations in flowering plants, and is characterized by failure in endosperm development and function, arrest in embryogenesis, and seed collapse. Many genetic components of triploid seed lethality have been successfully identified in the model plant Arabidopsis thaliana, most notably the paternally expressed imprinted genes (PEGs) that are up-regulated in the tetraploid endosperm with paternal excess. Previous studies have shown that the paternal epigenome is a key determinant of the triploid block response, as the loss of DNA methylation in diploid pollen suppresses the triploid block almost completely. Here, we demonstrate that triploid seed abortion is bypassed in plants treated with the DNA methyltransferase inhibitor 5-Azacytidine during seed germination and early plant growth. We have identified strong suppressor lines showing transgenerational inheritance of hypomethylation in CG context, as well as normalized expression of PEGs. Importantly, differentially methylated loci segregate in the progeny of "epimutagenized" plants, which may allow the identification of epialleles involved in the triploid block response in future studies. Finally, we demonstrate that chemically-induced epimutagenesis allows bypassing interploidy hybridizations in Arabidopsis and interspecific hybridization barriers in crosses between Capsella species, thus potentially emerging as a novel strategy for seed-based breeding of triploids and interspecific hybrids with agronomical interest.
2021-11-23 | GSE179697 | GEO
Project description:The "triploid block" prevents interploidy hybridizations in flowering plants, and is characterized by failure in endosperm development and function, arrest in embryogenesis, and seed collapse. Many genetic components of triploid seed lethality have been successfully identified in the model plant Arabidopsis thaliana, most notably the paternally expressed imprinted genes (PEGs) that are up-regulated in the tetraploid endosperm with paternal excess. Previous studies have shown that the paternal epigenome is a key determinant of the triploid block response, as the loss of DNA methylation in diploid pollen suppresses the triploid block almost completely. Here, we demonstrate that triploid seed abortion is bypassed in plants treated with the DNA methyltransferase inhibitor 5-Azacytidine during seed germination and early plant growth. We have identified strong suppressor lines showing transgenerational inheritance of hypomethylation in CG context, as well as normalized expression of PEGs. Importantly, differentially methylated loci segregate in the progeny of "epimutagenized" plants, which may allow the identification of epialleles involved in the triploid block response in future studies. Finally, we demonstrate that chemically-induced epimutagenesis allows bypassing interploidy hybridizations in Arabidopsis and interspecific hybridization barriers in crosses between Capsella species, thus potentially emerging as a novel strategy for seed-based breeding of triploids and interspecific hybrids with agronomical interest.
2021-11-23 | GSE179702 | GEO
Project description:Hybridization of diverged taxa often result in lethality or sterility. We previously described natural variation for postzygotic incompatibility in the cross of diploid Arabidopsis thaliana to Arabidopsis arenosa. Hybrid seed death in this system has a complex genetic basis, involving many non-additive interactions. While activation of AGAMOUS-LIKE genes (AGL) and Athila elements have been detected 5-8 days after pollination (DAP), the molecular basis of death remains mysterious. To address this problem, we compared 3DAP transcriptomes in interspecific hybrids from two A. thaliana ecotypes, one compatible, the other incompatible. Relative to self crosses of the respective A. thaliana seed parent, hybrids displayed differential expression of key developmental regulators in both the endosperm and maternal seed coat as well as natural variation for stress response genes. Ribosomal protein genes and a photosynthetic cluster of genes were hyperactivated, presumably in response to growth signals. Suppressing endosperm growth factor IKU1 and defense response regulators such as NON-EXPRESSOR OF PATHOGENESIS RELATED1 (NPR1) improved hybrid seed survival. Therefore, in incompatible hybrids disruption of seed development most likely initiates in the endosperm, rapidly affecting embryo and seed coat. The activation of putative POLYCOMB REPRESSIVE COMPLEX (PRC) gene targets, together with a twenty-fold reduction in expression of the FERTILIZATION INDEPENDENT SEED 2 gene, indicates a PRC role. Examination of differential gene expression of incompatible A. thaliana eco. Col-0 X A. arenosa and compatible A. thaliana eco. C24 X A. arenosa hybrid seeds plus corresponding A. thaliana and A. arenosa control crosses.
2013-06-05 | E-GEOD-42957 | biostudies-arrayexpress
Project description:Polyploidy, the presence of more than two sets of chromosomes within the nucleus, is a common phenomenon among plants that has shaped genome organization and is thought to be a major driver of speciation. The triploid block acts as a reproductive barrier that prevents successful backcrosses of newly formed polyploids with their progenitors. It is established in the endosperm, an ephemeral tissue that nurtures the developing embryo. Here we show that paternal 21/22 nucleotide epigenetically activated small interfering RNAs (easiRNAs) in Arabidopis thaliana are responsible for the establishment of the triploid block associated seed abortion. This dramatic phenotype is overcome when crosses are performed with a paternal mutant in the plant specific RNA polymerase IV (Pol IV). Loss of Pol IV reduces both easiRNAs and hetsiRNAs in the pollen grain. Seeds derived from crosses between wild type tetraploid fathers and diploid mothers have reduced levels of hetsiRNAs and cytosine methylation at transposable elements (TEs), indicating that they have suffered an excess of epigenetic reprogramming due to an excess of paternally derived easiRNAs. Paternal Pol IV mutants are able to buffer that easiRNA excess and rescue the abortion phenotype by rescuing both the cytosine methylation level at TEs and the 24 nt hetsiRNA accumulation levels. This mechanism highlights the elegant and important TE regulation mechanism controlled by the plant specific Pol IV that takes place pre-fertilization and regulates paternal easiRNAs and maternal hetsiRNAs, and determines the post-fertilization epigenetic stability and seed viability.
2017-12-14 | GSE84122 | GEO