Ontology highlight
ABSTRACT:
PROVIDER: PRJNA530263 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8840600_1.fastq.gz | Fastqsanger.gz | |||
| SRR8840600_2.fastq.gz | Fastqsanger.gz | |||
| SRR8840601_1.fastq.gz | Fastqsanger.gz | |||
| SRR8840601_2.fastq.gz | Fastqsanger.gz | |||
| SRR8840592_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:We described in this work the reproductive barrier between Capsella rubella and Capsella grandiflora leading to hybrid seed inviability. The transcriptome revealed a similar response to the one observed in interploidy hybrid seeds.
2015-03-28 | GSE67359 | 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
Project description:In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. Here, we find that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid-dysgenesis models, daughters show a markedly different content of piRNAs targeting each element, depending upon its parent of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are crucial for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis. Mappers table contains all of the sequences in our libraries that map to the drosophila genome (release 5) Nonmappers table contains all of the sequences in our libraries that do not map to the drosophila genome(release 5)
2008-11-28 | GSE13081 | GEO
Project description:The core promoter of protein-encoding genes plays a central role in regulating transcription. M1BP is a transcriptional activator that associates with a core promoter element known as Motif 1 that resides at thousand of genes in Drosophila. To gain insight into how M1BP functions, we identified an interacting protein called GFZF. GFZF had been previously identified in genetic screens for factors involved in maintenance of hybrid inviability, the G2-M DNA damage checkpoint, and RAS/MAPK signaling but its contribution to these processes was unknown. Previous evidence indicated that GFZF resides in the cytoplasm. Here, we show that GFZF resides in the nucleus and functions as a transcriptional co-activator. In addition, we show that GFZF is a glutathione S-transferase(GST). Thus, GFZF is the first transcriptional co-activator with intrinsic GST activity, and its identification as a transcriptional co-activator provides an explanation for its role in numerous biological processes.
2017-12-22 | GSE105009 | GEO
Project description:Evolution of hybrid inviability associated with chromosome fusions
| PRJEB69278 | ENA
Project description:In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. Here, we find that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid-dysgenesis models, daughters show a markedly different content of piRNAs targeting each element, depending upon its parent of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are crucial for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis. Mappers table contains all of the sequences in our libraries that map to the drosophila genome (release 5) Nonmappers table contains all of the sequences in our libraries that do not map to the drosophila genome(release 5) 15 small RNA libraries were generated from total RNA of Drosophila melanogaster ovarian and embryo tissues and analyzed for this study
2008-11-28 | E-GEOD-13081 | biostudies-arrayexpress
Project description:Hybridization of eggs and sperm from closely related species can give rise to genetic diversity, or can lead to embryo inviability due to incompatibility. Although central to evolution, the cellular and molecular mechanisms underlying postzygotic barriers that drive reproductive isolation and speciation remain largely unknown. Species of the African Clawed frog Xenopus provide an ideal system to study hybridization and genome evolution. Xenopus laevis is an allotetraploid with 36 chromosomes that arose through interspecific hybridization of diploid progenitors, whereas Xenopus tropicalis is a diploid with 20 chromosomes that diverged from a common ancestor ~48 million years ago. Differences in genome size between the two species are accompanied by organism size differences, and size scaling of the egg and subcellular structures such as nuclei and spindles formed in egg extracts. Nevertheless, early development transcriptional programs, gene expression patterns, and protein sequences are generally conserved. Interestingly, whereas the hybrid produced when X. laevis eggs are fertilized by X. tropicalis sperm (le×ts) is viable, the reverse hybrid (te×ls) dies prior to gastrulation. Here, we applied cell biological tools and high-throughput methods to study the mechanisms underlying hybrid inviability. We reveal that two specific X. laevis chromosomes are incompatible with the X. tropicalis cytoplasm and are mis-segregated during mitosis, leading to unbalanced gene expression at the maternal to zygotic transition, followed by cell-autonomous catastrophic embryo death.
2017-11-01 | GSE106157 | 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:Species of the genus Drosophila have served as favorite models in speciation studies, however genetic factors of the interspecific hybrid sterility are underinvestigated to date. Here we performed the analysis of reproductive incompatibilities of hybrid females in crossing Drosophila melanogaster females and Drosophila simulans males. Using transcriptomic data analysis, molecular, cellular and genetic approaches we analyzed differential gene expression, transposable element (TE) activity, piRNA biogenesis and functional defects of oogenesis in hybrids. A premature GSC loss was a most prominent defect of oogenesis in hybrid ovaries. Owing differential expression of genes encoding components of the piRNA pathway rhino and deadlock, functional RDCmel complex in hybrid ovaries was not assembled. At the same time the activity of RDCsim complex was maintained in hybrids, independently from the genomic origin of piRNA clusters. Despite identification of a cohort of overexpressed TEs in hybrid ovaries we found no evidences that their activity can be considered as the main cause of hybrid sterility. We revealed complex pattern of Vasa protein expression in hybrid germline, including partial AT-chX piRNA targeting of vasasim allele and significant developmental delay of vasamel expression. We came to the conclusions that complex multi-locus genetic changes between the species were responsible for hybrid sterility phenotype.
2024-05-30 | GSE263983 | GEO