Mimulus hybrid cultivar
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA715438 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14078400.fastq.gz | Fastqsanger.gz | |||
| SRR14078401.fastq.gz | Fastqsanger.gz | |||
| SRR14078402.fastq.gz | Fastqsanger.gz | |||
| SRR14078403.fastq.gz | Fastqsanger.gz | |||
| SRR14078404.fastq.gz | Fastqsanger.gz |
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Project description:The formation of new species is often a consequence of genetic incompatibilities accumulated between populations during allopatric divergence. When divergent taxa interbreed, these incompatibilities impact physiology and have a direct cost resulting in reduced hybrid fitness. Recent surveys of gene regulation in interspecific hybrids have revealed anomalous expression across large proportions of the genome, with 30-70% of all genes apparently misexpressed, mostly in the direction of down-regulation. However, since most of these studies have focused on pairs of species exhibiting high degrees of reproductive isolation, the association between regulatory disruption and reduced hybrid fitness prior to species formation remains unclear. Within the copepod species Tigriopus californicus, interpopulation hybrids show reduced fitness associated with mitochondrial dysfunction. Here we show that in contrast to studies of interspecific hybrids, only 1.2% of the transcriptome was misexpressed in interpopulation hybrids of T. californicus, and nearly 80% of misexpressed genes were overexpressed rather than underexpressed. Moreover, many of the misexpressed genes were components of functional pathways impacted by mitonuclear incompatibilities in hybrid T. californicus (e.g., oxidative phosphorylation and antioxidant response). We also show that the magnitude of hybrid misregulation is not dependent on levels of protein sequence divergence, even though the latter is correlated with expression divergence between parental populations. Our results suggest that hybrid breakdown at early stages of speciation may result from initial incompatibilities amplified by the cost of compensatory physiological responses.
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Project description:Dobzhansky-Muller incompatibilities represent a major driver of reproductive isolation between species. They are caused when two or more interacting components encoded by alleles from different species cannot function properly when mixed. At incipient stages of speciation, complex incompatibilities involving multiple genetic loci with weak effects are frequently observed, but the underlying mechanisms remain elusive. We observed perturbed proteostasis leading to compromised mitosis and meiosis in Saccharomyces cerevisiae hybrid lines carrying one or two chromosomes from Saccharomyces bayanus var uvarum. Levels of proteotoxicity are correlated with the number of protein complexes on replaced chromosomes and can be alleviated or aggravated, respectively, by up- or down-regulating the ubiquitin-proteasomal degradation machinery. Using proteomic approaches, we detect destabilized multi-protein complexes in a hybrid line. However, hybrid fitness can be significantly improved by rescuing small ribosomal subunits, a primary destabilized complex. Our findings reveal the general role of impaired protein complex assembly in complex incompatibilities.
2022-07-05 | PXD028358 | Pride
Project description:The formation of new species is often a consequence of genetic incompatibilities accumulated between populations during allopatric divergence. When divergent taxa interbreed, these incompatibilities impact physiology and have a direct cost resulting in reduced hybrid fitness. Recent surveys of gene regulation in interspecific hybrids have revealed anomalous expression across large proportions of the genome, with 30-70% of all genes apparently misexpressed, mostly in the direction of down-regulation. However, since most of these studies have focused on pairs of species exhibiting high degrees of reproductive isolation, the association between regulatory disruption and reduced hybrid fitness prior to species formation remains unclear. Within the copepod species Tigriopus californicus, interpopulation hybrids show reduced fitness associated with mitochondrial dysfunction. Here we show that in contrast to studies of interspecific hybrids, only 1.2% of the transcriptome was misexpressed in interpopulation hybrids of T. californicus, and nearly 80% of misexpressed genes were overexpressed rather than underexpressed. Moreover, many of the misexpressed genes were components of functional pathways impacted by mitonuclear incompatibilities in hybrid T. californicus (e.g., oxidative phosphorylation and antioxidant response). We also show that the magnitude of hybrid misregulation is not dependent on levels of protein sequence divergence, even though the latter is correlated with expression divergence between parental populations. Our results suggest that hybrid breakdown at early stages of speciation may result from initial incompatibilities amplified by the cost of compensatory physiological responses. Our experiment included nine RNA-seq samples: 3 San Diego, 2 Santa Cruz, and 4 hybrid samples. For each sample, 400-500 copepods across all developmental stages were collected from their stock cultures. They were transferred to fresh filtered seawater in a 50-mL Falcon tubes and immersed in a 20°C water bath for two hours. Water was then quickly removed, 4 mL of Tri-Reagent (Sigma) added, and tissue immediately disrupted using a tissue homogenizer. RNA was isolated following the manufacturer’s protocol. Re-suspended RNA pellets were further purified with RNeasy Mini columns (Qiagen), and final sample integrity and quantity were assessed with an Agilent 2100 BioAnalyzer. Please note that two samples (GSM1531288, GSM1531290) have been accessioned under BioProject PRJNA168170, SRA study SRP013608, while the remaining seven samples under BioProject PRJNA263967, SRA Study SRP048974. The current records including all 9 samples (PRJNA264820/SRP049247) were re-created for the convenient retrieval of the complete raw data from SRA
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Project description:Nymphaea hybrid endosperm, gene expression and DNA methylation characterization
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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.
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Project description:The Dobzhansky-Muller model provides a widely accepted mechanism for the evolution of reproductive isolation: incompatible substitutions disrupt interactions between genes. To date, few candidate incompatibility genes have been identified, leaving the genes driving speciation mostly uncharacterized. The importance of interactions in the Dobzhansky-Muller model suggests that gene coexpression networks provide a powerful framework to understand disrupted pathways associated with postzygotic isolation. Here, we perform Weighted Gene Coexpression Network Analysis (WGCNA) to infer gene interactions in hybrids of two recently diverged European house mouse subspecies, Mus mus domesticus and M. m. musculus, which commonly show hybrid male sterility or subfertility. We use genome-wide testis expression data from 467 hybrid mice from two mapping populations: F2s from a laboratory cross between wild-derived pure subspecies strains and offspring of natural hybrids captured in the Central Europe hybrid zone. This large data set enabled us to build a robust consensus network using hybrid males with fertile phenotypes. We identify several expression modules, or groups of coexpressed genes, that are disrupted in subfertile hybrids, including modules functionally enriched for spermatogenesis, cilium and sperm flagellum organization, chromosome organization and DNA repair, and including genes expressed in spermatogonia, spermatocytes and spermatids. Our network-based approach enabled us to hone in on specific hub genes likely to be influencing module-wide gene expression and hence potentially driving Dobzhansky-Muller incompatibilities. A total of 67 (24.4%) of these genes lie in sterility loci identified previously in these mapping populations, and represent promising candidate barrier genes and targets for future functional analysis.
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Project description:Hybrid seed lethality as a consequence of interspecies or interploidy hybridizations is a major mechanism of reproductive isolation in plants. This mechanism is manifested in the endosperm, a dosage sensitive tissue supporting embryo growth. Deregulated expression of imprinted genes like ADMETOS (ADM) underpin the interploidy hybridization barrier in Arabidopsis thaliana, however, the mechanisms of their action remained unknown. In this study we show that ADM interacts with the AT-hook domain protein AHL10 and the SET domain-containing SU(VAR)3-9 homolog SUVH9 and ectopically recruits the heterochromatic mark H3K9me2 to AT-rich transposable elements (TEs), causing deregulated expression of neighboring genes. Several hybrid incompatibility genes identified in Drosophila encode for heterochromatin-interacting proteins, which has led to the suggestion that hybrid incompatibilities evolve as consequence of interspecies divergence of selfish DNA elements and their regulation. Our data showing that imbalance of dosage-sensitive chromatin regulators underpins hybrid incompatibility in Arabidopsis strongly support this view, demonstrating that reproductive isolation as a consequence of epigenetic regulation of TEs is a conserved feature in animals and plants.
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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.
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