Lupinus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318864 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3422970_1.fastq.gz | Fastqsanger.gz | |||
| SRR3422970_2.fastq.gz | Fastqsanger.gz | |||
| SRR3422980_1.fastq.gz | Fastqsanger.gz | |||
| SRR3422980_2.fastq.gz | Fastqsanger.gz | |||
| SRR3423020_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 148 |
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Project description:Although the relationship between phenotypic plasticity and evolutionary dynamics has attracted large interest, very little is known about the contribution of phenotypic plasticity to adaptive evolution. In this study, we analyzed phenotypic and genotypic changes in E. coli cells during adaptive evolution to ethanol stress. To quantify the phenotypic changes, transcriptome analyses were performed.
2014-07-21 | GSE59050 | GEO
Project description:<p>Understanding metabolic plasticity of animal evolution is a fundamental challenge in evolutionary biology. Owing to the diversification of insect wing morphology and dynamic energy requirements, the molecular adaptation mechanisms underlying the metabolic pathways in wing evolution remain largely unknown. This study reveals the pivotal role of the duplicated Apolipoprotein D (ApoD) gene in lipid and energy homeostasis in the lepidopteran wing. ApoD underwent significant expansion in insects, with gene duplication and consistent retention observed in Lepidoptera. Notably, duplicated ApoD2 was highly expressed in lepidopteran wings and encoded a unique C-terminal tail, conferring distinct ligand-binding properties. Using Bombyx mori as a model system, we integrated evolutionary analysis, multiomics, and in vivo functional experiments to elucidate the way duplicated ApoD2 mediates lipid trafficking and homeostasis via the AMP-activated protein kinase pathway in wings. Moreover, we revealed the specific expression and functional divergence of duplicated ApoD as a key mechanism regulating juvenile hormone levels and lipid homeostasis in the lepidopteran wing. These findings highlight an evolutionary scenario in which functional divergence and neofunctionalization conferred a novel role of ApoD in shaping adaptive lipid metabolic regulatory networks during wing phenotypic evolution. Overall, we provide in vivo evidence for the functional differentiation of duplicate genes in shaping adaptive metabolic regulatory networks during phenotypic evolution.</p>
2026-03-29 | MTBLS4308 | MetaboLights
Project description:<p>Understanding metabolic plasticity of animal evolution is a fundamental challenge in evolutionary biology. Owing to the diversification of insect wing morphology and dynamic energy requirements, the molecular adaptation mechanisms underlying the metabolic pathways in wing evolution remain largely unknown. This study reveals the pivotal role of the duplicated Apolipoprotein D (ApoD) gene in lipid and energy homeostasis in the lepidopteran wing. ApoD underwent significant expansion in insects, with gene duplication and consistent retention observed in Lepidoptera. Notably, duplicated ApoD2 was highly expressed in lepidopteran wings and encoded a unique C-terminal tail, conferring distinct ligand-binding properties. Using Bombyx mori as a model system, we integrated evolutionary analysis, multiomics, and in vivo functional experiments to elucidate the way duplicated ApoD2 mediates lipid trafficking and homeostasis via the AMP-activated protein kinase pathway in wings. Moreover, we revealed the specific expression and functional divergence of duplicated ApoD as a key mechanism regulating juvenile hormone levels and lipid homeostasis in the lepidopteran wing. These findings highlight an evolutionary scenario in which functional divergence and neofunctionalization conferred a novel role of ApoD in shaping adaptive lipid metabolic regulatory networks during wing phenotypic evolution. Overall, we provide in vivo evidence for the functional differentiation of duplicate genes in shaping adaptive metabolic regulatory networks during phenotypic evolution.</p>
2026-03-29 | MTBLS11285 | MetaboLights
Project description:Although the relationship between phenotypic plasticity and evolutionary dynamics has attracted large interest, very little is known about the contribution of phenotypic plasticity to adaptive evolution. In this study, we analyzed phenotypic and genotypic changes in E. coli cells during adaptive evolution to ethanol stress. To quantify the phenotypic changes, transcriptome analyses were performed. We previously obtained 6 independently evolved ethanol tolerant E. coli strains, strains A through F, by culturing cells under 5% ethanol stress for about 1000 generations and found a significantly larger growth rate than the parent strains (Horinouchi et al, 2010, PMID: 20955615). To elucidate the phenotypic changes that occurred during adaptive evolution, we quantified the time-series of the expression changes by microarray analysis. Starting from frozen stocks obtained at 6 time points (0, 384, 744, 1224, 1824 and 2496 hours) in laboratory evolution, cells were cultured under 5% ethanol stress, and mRNA samples were obtained in the exponential growth phase for microarray analysis.
2014-07-21 | E-GEOD-59050 | biostudies-arrayexpress
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2013-11-28 | E-GEOD-52786 | biostudies-arrayexpress
Project description:One of the central goals of evolutionary biology is to explain and predict the molecular basis of adaptive evolution. We studied the evolution of genetic networks in Saccharomyces cerevisiae (budding yeast) populations propagated for more than 200 generations in different nitrogen-limiting conditions. We find that rapid adaptive evolution in nitrogen-poor environments is dominated by the de novo generation and selection of copy number variants (CNVs), a large fraction of which contain genes encoding specific nitrogen transporters including PUT4, DUR3 and DAL4. The large fitness increases associated with these alleles limits the genetic heterogeneity of adapting populations even in environments with multiple nitrogen sources. Complete identification of acquired point mutations, in individual lineages and entire populations, identified heterogeneity at the level of genetic loci but common themes at the level of functional modules, including genes controlling phosphatidylinositol-3-phosphate metabolism and vacuole biogenesis. Adaptive strategies shared with other nutrient-limited environments point to selection of genetic variation in the TORC1 and Ras/PKA signaling pathways as a general mechanism underlying improved growth in nutrient-limited environments. Within a single population we observed the repeated independent selection of a multi-locus genotype, comprised of the functionally related genes GAT1, MEP2 and LST4. By studying the fitness of individual alleles, and their combination, as well as the evolutionary history of the evolving population, we find that the order in which these mutations are acquired is constrained by epistasis. The identification of repeatedly selected variation at functionally related loci that interact epistatically suggests that gene network polymorphisms (GNPs) may be a frequent outcome of adaptive evolution. Our results provide insight into the mechanistic basis by which cells adapt to nutrient-limited environments and suggest that knowledge of the selective environment and the regulatory mechanisms important for growth and survival in that environment greatly increases the predictability of adaptive evolution. DNA from each evolved clone or population is hybridized vs DNA from the ancestral strain
2013-11-28 | E-GEOD-52696 | biostudies-arrayexpress
Project description:Gene copy-number variation, which provides the raw material for the evolution of novel genes, is surprisingly widespread in natural populations. Experimental evolution studies have demonstrated an extremely high spontaneous rate of origin of gene duplications. When organisms are suboptimally adapted to their environment, gene duplication may compensate for reduced fitness by amplifying promiscuous activity of a gene, or increasing dosage of a suboptimal gene. The overarching goal of this study is to inverstigate whether CNVs constitute a common mechanism of adaptive genetic change during compensatory evolution and to further characterize the role of natural selection in dictating their evolutionary spread at a population-genomic level. Outcrossing populations of C. elegans with low fitness were evolved for >200 generations and the frequencies of CNVs in these populations were analyzed by oligonucleotide array comparative genome hybridization, quantitative PCR, and single-worm PCR. Multiple duplications and deletions were detected in intermediate to high frequencies and several lines of evidence suggest that the changes in frequency were adaptive. 1) Many copy-number changes reached high frequency, were near fixation, or were fixed in a short time. 2) Many independent duplications and deletions in high frequency harbor overlapping regions which likely include genes that are under selection for either higher or lower rates of expression. 3) The size spectrum of deuplications and deletions in the adaptive recovery populations is significantly larger than that of spontaneous copy-number variants in mutation accumulation experiments. This is expected if larger CNVs are more likely to encompass genes that are being selected for altered gene dosage. Out results validate the great potential borne by gene copy-number changes for compensatory evolution and adaptation. Experimental genome evolution of copy-number variants in 25 experimental lines compared to 5 ancestral control lines.
2015-04-15 | E-GEOD-67871 | biostudies-arrayexpress
Project description:One of the central goals of evolutionary biology is to explain and predict the molecular basis of adaptive evolution. We studied the evolution of genetic networks in Saccharomyces cerevisiae (budding yeast) populations propagated for more than 200 generations in different nitrogen-limiting conditions. We find that rapid adaptive evolution in nitrogen-poor environments is dominated by the de novo generation and selection of copy number variants (CNVs), a large fraction of which contain genes encoding specific nitrogen transporters including PUT4, DUR3 and DAL4. The large fitness increases associated with these alleles limits the genetic heterogeneity of adapting populations even in environments with multiple nitrogen sources. Complete identification of acquired point mutations, in individual lineages and entire populations, identified heterogeneity at the level of genetic loci but common themes at the level of functional modules, including genes controlling phosphatidylinositol-3-phosphate metabolism and vacuole biogenesis. Adaptive strategies shared with other nutrient-limited environments point to selection of genetic variation in the TORC1 and Ras/PKA signaling pathways as a general mechanism underlying improved growth in nutrient-limited environments. Within a single population we observed the repeated independent selection of a multi-locus genotype, comprised of the functionally related genes GAT1, MEP2 and LST4. By studying the fitness of individual alleles, and their combination, as well as the evolutionary history of the evolving population, we find that the order in which these mutations are acquired is constrained by epistasis. The identification of repeatedly selected variation at functionally related loci that interact epistatically suggests that gene network polymorphisms (GNPs) may be a frequent outcome of adaptive evolution. Our results provide insight into the mechanistic basis by which cells adapt to nutrient-limited environments and suggest that knowledge of the selective environment and the regulatory mechanisms important for growth and survival in that environment greatly increases the predictability of adaptive evolution.
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Project description:One of the central goals of evolutionary biology is to explain and predict the molecular basis of adaptive evolution. We studied the evolution of genetic networks in Saccharomyces cerevisiae (budding yeast) populations propagated for more than 200 generations in different nitrogen-limiting conditions. We find that rapid adaptive evolution in nitrogen-poor environments is dominated by the de novo generation and selection of copy number variants (CNVs), a large fraction of which contain genes encoding specific nitrogen transporters including PUT4, DUR3 and DAL4. The large fitness increases associated with these alleles limits the genetic heterogeneity of adapting populations even in environments with multiple nitrogen sources. Complete identification of acquired point mutations, in individual lineages and entire populations, identified heterogeneity at the level of genetic loci but common themes at the level of functional modules, including genes controlling phosphatidylinositol-3-phosphate metabolism and vacuole biogenesis. Adaptive strategies shared with other nutrient-limited environments point to selection of genetic variation in the TORC1 and Ras/PKA signaling pathways as a general mechanism underlying improved growth in nutrient-limited environments. Within a single population we observed the repeated independent selection of a multi-locus genotype, comprised of the functionally related genes GAT1, MEP2 and LST4. By studying the fitness of individual alleles, and their combination, as well as the evolutionary history of the evolving population, we find that the order in which these mutations are acquired is constrained by epistasis. The identification of repeatedly selected variation at functionally related loci that interact epistatically suggests that gene network polymorphisms (GNPs) may be a frequent outcome of adaptive evolution. Our results provide insight into the mechanistic basis by which cells adapt to nutrient-limited environments and suggest that knowledge of the selective environment and the regulatory mechanisms important for growth and survival in that environment greatly increases the predictability of adaptive evolution.
2013-11-28 | GSE52786 | GEO
Project description:Adaptive evolution is generally assumed to progress through the accumulation of beneficial mutations. However, deleterious mutations may also have an important role by promoting adaptive genetic changes that are otherwise inaccessible. Here we study the capacity of the bakerM-bM-^@M-^Ys yeast genome to compensate the complete loss of genes during evolution, and explore the long-term consequences of this process. We initiated laboratory evolutionary experiments with over 180 haploid yeast genotypes, all of which initially displayed slow growth due to the deletion of a single gene. Compensatory adaptation was rapid and pervasive, and it promoted the genomic divergence of parallel evolving populations. The accumulated mutations did not restore wild type genomic expression states and generated diverse growth phenotypes across environments. Taken together, gene loss initiates genomic changes that can influence evolutionary potential upon environmental change. Evolved yeast-lines were generated by growing strains for 400 doublings during 104 days on YPD medium in 96 wells plates, 8 evolved lines were selected for microarray analysis. Two independent colonies of the wild type control, evolved and corresponding ancestor knock-out strains were grown to early midlog and used for transcription profiling by dual channel array against a common reference.
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