Ontology highlight
ABSTRACT:
PROVIDER: PRJNA641718 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12108816.fastq.gz | Fastqsanger.gz | |||
| SRR12108816_1.fastq.gz | Fastqsanger.gz | |||
| SRR12108816_2.fastq.gz | Fastqsanger.gz | |||
| SRR12108817_1.fastq.gz | Fastqsanger.gz | |||
| SRR12108817_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 29 |
Similar Datasets
Project description:A comprehensive genotype-fitness map of adaptation-driving mutations in yeast
| PRJNA310010 | ENA
Project description:The intrinsic complexity of quantitative traits was evident even before the molecular nature of the gene was understood. Yet we still lack a detailed molecular understanding of complex heritability. Here we alleviated statistical roadblocks to high-resolution genetic mapping by using an inbred population of diploid yeast with very low linkage disequilibrium and more individuals than segregating polymorphisms. We mapped over 18,000 quantitative trait loci, resolving more than 3,300 to single nucleotides. This allowed us to explore the molecular origins of complexity, hybrid vigor, pleiotropy, and gene ´ environment interactions and to rigorously estimate the distribution of fitness effects of natural genetic variation. Our results describe a comprehensive, high-resolution genotype-to-phenotype map and define general principles underlying the complexity of heredity.
2018-12-13 | GSE123702 | GEO
Project description:Geographically distinct populations can adapt to the temperature conditions of their local environment, leading to temperature-dependent fitness differences between populations. Consistent with local adaptation, phylogeographically distinct Caenorhabditis briggsae nematodes show distinct fitness responses to temperature. The genetic mechanisms underlying local adaptation, however, remain unresolved. To investigate the potential role of small noncoding RNAs in genotype-specific responses to temperature, we quantified small RNA expression using high-throughput sequencing of C. briggsae nematodes from tropical and temperate strain genotypes reared under three temperature conditions (14˚, 20˚, 30˚C). Strains representing both tropical and temperate regions showed significantly lower expression of PIWI-interacting RNAs (piRNAs) at high temperatures, primarily mapping to a large ~7 Mb long piRNA cluster on chromosome IV. We also documented decreased expression of 22G-RNAs antisense to protein-coding genes and other genomic features at high rearing temperatures for the thermally-intolerant temperate strain genotype, but not for the tropical strain genotype. Reduced 22G-RNA expression was widespread along chromosomes and among feature types, indicative of a genome-wide response. Targets of the EGO-1/CSR-1 22G-RNA pathway were most strongly impacted compared to other 22G-RNA pathways, implicating the CSR-1 Argonaute and its RNA-dependent RNA polymerase EGO-1 in the genotype-dependent modulation of C. briggsae 22G-RNAs under chronic thermal stress. Our work suggests that gene regulation via small RNAs may be an important contributor to the evolution of local adaptations.
2022-05-22 | GSE202589 | GEO
Project description:BACKGROUND:Isobutanol is a promising next generation biofuel with demonstrated high yield microbial production, but the toxicity of this molecule reduces fermentation volumetric productivity and final titers. Organic solvent tolerance is a complex, multigenic phenotype that has been recalcitrant to rational engineering approaches. We apply experimental evolution followed by genome resequencing and a gene expression study to elucidate genetic bases on adaptation to exogenous isobutanol stress. RESULTS:The adaptations acquired in our evolved lineages exhibit antagonistic pleiotropy between minimal and rich medium, and appear to be specific to the effects of longer chain alcohols. By examining genotypic adaptation in multiple independent lineages, we find evidence of parallel evolution in hfq, mdh, acrAB, gatYZABCD, and rph genes. Many isobutanol tolerant lineages show reduced rpoS activity, perhaps related to mutations in hfq or acrAB. Consistent with the complex, multigenic nature of solvent tolerance, we observe adaptations in a diversity of cellular processes. Many adaptations appear to involve epistasis between different mutations, implying a rugged fitness landscape for isobutanol tolerance. We observe a trend of evolution targeting post-transcriptional regulation and high centrality nodes of biochemical networks. Collectively, the genotypic adaptations we observe suggest mechanisms of adaptation to isobutanol stress based on remodelling the cell envelope and surprisingly, stress response attenuation. CONCLUSIONS:We have discovered a set of genotypic adaptations that confer increased tolerance to exogenous isobutanol stress. Our results are immediately useful to efforts to engineer more isobutanol tolerant host strains of E. coli for isobutanol production. We suggest that rpoS and post-transcriptional regulators, such as hfq, RNA helicases, and sRNAs may be interesting mutagenesis targets for futurue global phenotype engineering. Two strains (WT strain and G3.2 mutant strain), each with two culture conditions (with and without isobutanol in medium). Three biological replicates for each strain/culture condition. Twelve samples in total.
2010-08-10 | E-GEOD-23526 | biostudies-arrayexpress
Project description:BACKGROUND:Isobutanol is a promising next generation biofuel with demonstrated high yield microbial production, but the toxicity of this molecule reduces fermentation volumetric productivity and final titers. Organic solvent tolerance is a complex, multigenic phenotype that has been recalcitrant to rational engineering approaches. We apply experimental evolution followed by genome resequencing and a gene expression study to elucidate genetic bases on adaptation to exogenous isobutanol stress. RESULTS:The adaptations acquired in our evolved lineages exhibit antagonistic pleiotropy between minimal and rich medium, and appear to be specific to the effects of longer chain alcohols. By examining genotypic adaptation in multiple independent lineages, we find evidence of parallel evolution in hfq, mdh, acrAB, gatYZABCD, and rph genes. Many isobutanol tolerant lineages show reduced rpoS activity, perhaps related to mutations in hfq or acrAB. Consistent with the complex, multigenic nature of solvent tolerance, we observe adaptations in a diversity of cellular processes. Many adaptations appear to involve epistasis between different mutations, implying a rugged fitness landscape for isobutanol tolerance. We observe a trend of evolution targeting post-transcriptional regulation and high centrality nodes of biochemical networks. Collectively, the genotypic adaptations we observe suggest mechanisms of adaptation to isobutanol stress based on remodelling the cell envelope and surprisingly, stress response attenuation. CONCLUSIONS:We have discovered a set of genotypic adaptations that confer increased tolerance to exogenous isobutanol stress. Our results are immediately useful to efforts to engineer more isobutanol tolerant host strains of E. coli for isobutanol production. We suggest that rpoS and post-transcriptional regulators, such as hfq, RNA helicases, and sRNAs may be interesting mutagenesis targets for futurue global phenotype engineering.
2010-08-10 | GSE23526 | GEO
Project description:In order to study the effects of a mutation to the transcriptional termination regulator Rho (referred to as rho*), we made use of expression microarrays to observe the direct and indirect effects of rho* on gene expression. In addition, we used arrays to map the fitness of strains from transposon mutagenized libraries under four conditions, showing that in each case the majority of genes with significant fitness effects were dependent on the genotype at rho.
2012-06-01 | GSE32022 | GEO
Project description:Genotype-phenotype-epiphenotype analysis to decipher severity, penetrance, pleiotropy and mechanisms in CHD8-related neurodevelopmental disorder
| PRJNA1148667 | ENA
Project description:A fine scale phenotype-genotype virulence map of a bacterial pathogen
| PRJNA167605 | ENA