Ontology highlight
ABSTRACT:
PROVIDER: PRJNA739535 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR14876153.fastq.gz | Fastqsanger.gz | |||
| SRR14876154.fastq.gz | Fastqsanger.gz | |||
| SRR14876155.fastq.gz | Fastqsanger.gz | |||
| SRR14876156.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:Transcript abundance was measured in whole-body virgin male Drosophila serrata from 41 inbred lines that had diverged through 27 generations of mutation accumulation that were sexually selected Sexual selection is predicted to have widespread effects on the genetic variation generated by new mutations as a consequence of the genic capture of condition by male sexual traits. We manipulated the opportunity for sexual selection on males during 27 generations of mutation accumulation in inbred lines of Drosophila serrata, and used a microarray platform to investigate the effect of sexual selection on the expression of 2685 genes, representing a broad coverage of biological function. Sexual selection had little effect on mean gene expression levels, with only 4 genes diverging significantly at a false discovery rate of 5% . In contrast, sexual selection impacted on both the magnitude and nature of mutational variance accumulating in these genes. The magnitude of mutational variance increased under sexual selection by an average of 29%. Mutational variance was less commonly generated by extreme phenotypes less commonly under sexual selection. Furthermore, analysis of random sets of five genes revealed that the mutational variance that accumulated under sexual selection was less pleiotropic in nature than that found in the absence of sexual selection. The generation of greater mutational variance without a general concomitant change in mean expression under sexual selection suggested that gene expression traits were be under apparent rather than direct sexual selection. We discuss two main explanations for the broad-based increase in mutational variance under sexual selection that both require extensive pleiotropy between traits affecting male mating success, standard metric traits represented here by gene expression traits, and general fitness. We measured gene expression of male Drosophila serrata from 41 mutation accumulation lines (whole-body) that were sexually selected. Data from two replicates for each line are presented.
2014-03-01 | E-GEOD-54777 | biostudies-arrayexpress
Project description:Sexual selection on males is predicted to have widespread effects on genetic variation as a consequence of the pleiotropic allelic effects on sexual and non-sexual traits. We manipulated the opportunity for sexual selection on males during 27 generations of mutation accumulation in inbred lines of Drosophila serrata, and used a microarray platform to investigate the effect of sexual selection on the expression of 2689 genes. While gene expression signal was, on average, higher in the absence of sexual selection, this difference was small (0.1%). In contrast, sexual selection impacted substantially on the mutational variance in gene expression. Over all genes, mutational variance in gene expression was, on average, 42% higher when sexual selection operated than when it was absent. Our results indicate that sexual selection on males can generate widespread effects across the genome. An increase in mutational variance without a corresponding change in mean suggested that most expression traits were unlikely to be under direct sexual selection. Instead, the mutational variance in gene expression traits is consistent with divergence generated by widespread pleiotropic associations with traits affecting male mating success.
2014-03-01 | GSE54777 | GEO
Project description:Analysis of human fecal metagenomes from adults and infants, to investigate strain persistance, dispersal and purifying selection of bacterial strains.
| PRJEB41102 | ENA
Project description:The role natural selection plays in governing the locations and early evolution of copy number mutations remains largely unexplored. Here we employ high-density full-genome tiling arrays to create a fine-scale genomic map of copy number polymorphisms (CNPs) in Drosophila melanogaster. We inferred a total of 2,658 independent CNPs, 56% of which overlap genes. These include CNPs likely to be under positive selection, most notably high frequency duplications encompassing toxin-response genes. The locations and frequencies of CNPs are strongly shaped by purifying selection with deletions under stronger purifying selection than duplications. Among duplications, those overlapping exons or introns and those falling on the X-chromosome seem to be subject to the strongest purifying selection. In order to characterize copy number polymorphisms (CNPs) in Drosophila malanogaster, we applied comparative genome hybridization (CGH) using tiling arrays covering the full euchromatic genome of Drosophila melanogaster. We inferred copy number changes with a Hidden Markov Model (HMM) that returned the posterior probabilities for copy number by comparing DNA hybridization intensities between natural isolates and the reference genome strain. Training data for copy number changes were obtained via hybridization with a line known to contain a ~200kb homozygous duplication and from a set of 52 validated homozygous deletions. The probabilities of mutation were parsed to make CNP calls. Key words: comparative genomic hybridization, CGH, copy number polymorphism, CNP, copy number variation, CNV, duplication, deletion
2008-06-06 | GSE11326 | GEO
Project description:Plant Y-chromosome degeneration is retarded by haploid purifying selection.
| PRJNA146235 | ENA
Project description:The global transcriptional regulator Hha of Escherichia coli controls hemolysin activity, biofilm formation, and virulence expressions. Earlier, we have reported that Hha represses initial biofilm formation and disperses biofilms as well as controls prophage excision in E. coli. Since biofilm dispersal is a promising area to control biofilms, here we rewired Hha to control biofilm dispersal and formation. The Hha variant Hha13D6 was obtained to have enhanced biofilm dispersal activity along with increased toxicity compared to wild-type Hha (Hha13D6 induces dispersal 60%, whereas wild-type Hha induces dispersal at early biofilms but not at mature biofilms). Toxic Hha13D6 caused cell death probably by the activation of proteases HslUV, Lon, and PrlC, and deletion of protease gene hslV with overproducing Hh13D6 repressed biofilm dispersal, indicating Hha13D6 induces biofilm dispersal through the activity of protease HslV. Furthermore, another Hha variant Hha24E9 was also obtained to decrease biofilm formation 4-fold compared to wild-type Hha by regulation of gadW, glpT, and phnF. However, the dispersal variant Hha13D6 did not decrease biofilm formation, while the biofilm variant Hha24E9 did not induce biofilm dispersal. Hence, Hha may have evolved two ways in response to environmental factors to control biofilm dispersal and formation, but both controlling mechanisms come from different regulatory systems.
2010-10-31 | GSE21604 | GEO
Project description:The experimental approach seeks to test for sexual dimorphism in exuded non-volatile metabolites in C. purpureus. The proposed research is creative and original both in its inter-disciplinary approach and its use of a biochemically tractable phenotype to develop a much-needed link between natural selection for sexual dimorphism and the molecular targets of that selection pressure.
2015-07-01 | ST000239 | MetabolomicsWorkbench
Project description:The global transcriptional regulator Hha of Escherichia coli controls hemolysin activity, biofilm formation, and virulence expressions. Earlier, we have reported that Hha represses initial biofilm formation and disperses biofilms as well as controls prophage excision in E. coli. Since biofilm dispersal is a promising area to control biofilms, here we rewired Hha to control biofilm dispersal and formation. The Hha variant Hha13D6 was obtained to have enhanced biofilm dispersal activity along with increased toxicity compared to wild-type Hha (Hha13D6 induces dispersal 60%, whereas wild-type Hha induces dispersal at early biofilms but not at mature biofilms). Toxic Hha13D6 caused cell death probably by the activation of proteases HslUV, Lon, and PrlC, and deletion of protease gene hslV with overproducing Hh13D6 repressed biofilm dispersal, indicating Hha13D6 induces biofilm dispersal through the activity of protease HslV. Furthermore, another Hha variant Hha24E9 was also obtained to decrease biofilm formation 4-fold compared to wild-type Hha by regulation of gadW, glpT, and phnF. However, the dispersal variant Hha13D6 did not decrease biofilm formation, while the biofilm variant Hha24E9 did not induce biofilm dispersal. Hence, Hha may have evolved two ways in response to environmental factors to control biofilm dispersal and formation, but both controlling mechanisms come from different regulatory systems. For the whole-transcriptome study of BW25113 hha/pCA24N-hha13D6 versus BW25113 hha/pCA24N-hha biofilm dispersal, cells were grown in 250 mL of LB glucose (0.2%) for 16 h at 125 rpm with 10 g of glass wool (Corning Glass Works, Corning, NY, USA) in 1 L Erlenmeyer flasks to form a robust biofilm (Ren et al., 2004) and incubated an additional 1 h with 1 mM IPTG to induce wild-type Hha and Hha13D6. Similarly, for the whole transcriptome study of BW25113 hha/pCA24N-hha24E9 versus BW25113 hha/pCA24N-hha biofilm formation, cells were grown in 250 mL of LB glucose (0.2%) containing 1 mM IPTG for 7 h at 250 rpm with 10 g of glass wool to form biofilms. Biofilm cells were obtained by rinsing and sonicating the glass wool in sterile 0.85% NaCl solution at 0°C, and RNALater buffer® (Applied Biosystems, Foster City, CA, USA) was added to stabilize RNA during the RNA preparation steps. Total RNA was isolated from biofilm cells using a bead beater (Biospec, Bartlesville, OK, USA). cDNA synthesis, fragmentation, and hybridizations to the E. coli GeneChip Genome 2.0 array (Affymetrix, Santa Clara, CA, USA; P/N 511302). Genes were identified as differentially expressed if the expression ratio was higher than the standard deviation: 2.0-fold (induced and repressed) cutoff for Hha13D6 DNA microarrays (standard deviation 1.3-fold) and 10.0-fold (induced) or 4.0-fold (repressed) for Hha24E9 DNA microarrays (standard deviation 4.0-fold), and if the p-value for comparing two chips was less than 0.05.
2010-10-31 | E-GEOD-21604 | biostudies-arrayexpress
Project description:The experimental approach seeks to test for sexual dimorphism in exuded non-volatile metabolites in C. purpureus. The proposed research is creative and original both in its inter-disciplinary approach and its use of a biochemically tractable phenotype to develop a much-needed link between natural selection for sexual dimorphism and the molecular targets of that selection pressure.
2018-08-02 | MSV000082682 | GNPS
Project description:Social interactions are typically characterised by conflict and competition. This antagonism can play a critical role in evolutionary processes, such as promoting diversity through maintenance of alternative strategies or driving accelerated evolution through arms-race like escalation. However, despite our sophisticated understanding of how conflict shapes social traits, we still have limited knowledge of how it impacts molecular evolution across the underlying ‘social genes’. To address this problem, we analysed the genome wide impact of social interactions in a microbe. To understand broad-scale processes shaping molecular evolution at social genes we have used four different, but complementary, approaches to identify sets of social genes. For ease, we have named these sets ‘sociality’, ‘chimerism’, ‘antagonism’ and ‘cheater’ genes. Chimerism genes are defined as those up-regulated in chimeric aggregations in comparison to clonal aggregations. This is based on the logic that chimeric development will be characterised by conflict, and hence these genes will show the signatures of conflict driven evolution. Using genome sequences from 67 Dictyostelium discoideum strains, we find that social genes often exhibit enhanced polymorphism and accelerated evolution. However, these patterns are not consistent with the expectation of conflict driven processes, but instead reflect relatively relaxed purifying selection. This pattern reflects the fact that social interactions are conditional, and therefore selection on genes expressed in social interactions is diluted by generations of inactivity. This results in the ‘Red King’ process, wherein dilution of selection by inactivity enhances the role of drift, resulting in increased polymorphism and accelerated evolution.
2019-05-09 | GSE118081 | GEO