Ontology highlight
ABSTRACT:
PROVIDER: PRJNA589724 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The genomes of many vertebrates show a characteristic variation in GC content. To explain its origin and evolution mainly three mechanisms have been proposed, selection for GC content, mutation bias and GC-biased gene conversion. At present the mechanism of GC-biased gene conversion, i.e. short-scale, unidirectional exchanges between homologous chromosomes in the neighborhood of recombination-initiating double-strand breaks in favor for GC nucleotides, is the most widely accepted hypothesis. We here suggest that DNA methylation also plays an important role in the evolution of GC content in vertebrate genomes. To test this hypothesis we investigated one mammalian (human; GSE30340) and one avian (chicken) genome. We used bisulfite sequencing to generate a whole-genome methylation map of chicken sperm. Human processed data files (spermdonor1, #reads>=1) were downloaded from the NGSmethDB database (http://bioinfo2.ugr.es/NGSmethDB/database.php). Inclusion of these methylation maps into a model of GC content evolution provided significant support for the impact of DNA methylation on the local equilibrium GC content. Moreover, two different estimates of equilibrium GC content, one which neglects and one which incorporates the impact of DNA methylation and the concomitant CpG hypermutability, give estimates that differ about 15% in both genomes, arguing for a strong impact of DNA methylation on the evolution of GC content. Thus, our results put forward that previous estimates of equilibrium GC content, which neglect the hypermutability of CpG dinucleotides, need to be reevaluated. Genomic DNA from chicken mature sperm was isolated, bisulfite converted and sequenced on a Illumina HiSeq instrument
2015-01-23 | E-GEOD-56639 | biostudies-arrayexpress
Project description:Wolbachia pipientis is a worldwide bacterial parasite of arthropods that infects host germline cells and manipulates host reproduction to increase the ratio of infected females, the transmitting sex of the bacteria. The most common reproductive manipulation, cytoplasmic incompatibility (CI), is expressed as embryonic death in crosses between infected males and uninfected females. Specifically, Wolbachia modify developing sperm in the testes by unknown means to cause a post-fertilization disruption of the sperm chromatin that incapacitates the first mitosis of the embryo. As these Wolbachia-induced changes are stable, reversible, and affect the host cell cycle machinery including DNA replication and chromosome segregation, we hypothesized that the host methylation pathway is targeted for modulation during cytoplasmic incompatibility because it accounts for all of these traits. Here we show that infection of the testes is associated with a 55% increase of host DNA methylation in Drosophila melanogaster, but methylation of the paternal genome does not correlate with penetrance of CI. Overexpression and knock out of the Drosophila DNA methyltransferase Dnmt2 neither induces nor increases cytoplasmic incompatibility. Instead, overexpression decreases Wolbachia titers in host testes by approximately 17%, leading to a similar reduction in CI levels. Finally, strength of CI induced by several different strains of Wolbachia does not correlate with levels of DNA methylation in the host testes. We conclude that DNA methylation mediated by Drosophila's only known methyltransferase is not required for the transgenerational sperm modification that causes CI. Genomic DNA was extracted from pooled samples of Drosophila melanogaster adult testes. One sample from Wolbachia-infected males and one from uninfected males. Bisulfite sequencing was used to determine whether Wolbachia infection affects host DNA methylation in the testes.
2014-12-03 | E-GEOD-63795 | biostudies-arrayexpress
Project description:DNA methylation is a conserved epigenetic mark in plants and many animals. How parental alleles interact in progeny to influence the epigenome is poorly understood. We analyzed the DNA methylomes of Arabidopsis Col and C24 ecotypes, and their hybrid progeny. Hy- brids displayed nonadditive DNA methylation levels, termed meth- ylation interactions, throughout the genome. Approximately 2,500 methylation interactions occurred at regions where parental DNA methylation levels are similar, whereas almost 1,000 were at differ- entially methylated regions in parents. Methylation interactions were characterized by an abundance of 24-nt small interfering RNAs. Furthermore, dysfunction of the RNA-directed DNA methylation pathway abolished methylation interactions but did not affect the increased biomass observed in hybrid progeny. Methylation interac- tions correlated with altered genetic variation within the genome, suggesting that they may play a role in genome evolution. Whole genome bisulfite sequencing and small RNA sequencing of the wild type and nrpd1nrpe1 double mutant background of parent Col ,C24, the hybrid ColXC24 and C24XCol to explore the role of the RdDM pathway in DNA methylation interactions.
2016-06-15 | E-GEOD-72993 | biostudies-arrayexpress
Project description:Genetic variation is regarded as a prerequisite for evolution. Theoretical models suggest epigenetic information inherited independently of DNA sequence can also enable evolution. However, whether epigenetic inheritance mediates phenotypic evolution in natural populations is unknown. Here we show that natural epigenetic DNA methylation variation in gene bodies regulates genes expression, and thereby influences the natural variation of complex traits in Arabidopsis thaliana. Notably, the effects of methylation variation on phenotypic diversity and gene expression variance are comparable with those of DNA sequence polymorphism. We also identify methylation epialleles in numerous genes associated with environmental conditions in native habitats, suggesting that intragenic methylation facilitates adaptation to fluctuating environments. Our results demonstrate that methylation variation fundamentally shapes phenotypic diversity in natural populations and provides an epigenetic basis for adaptive Darwinian evolution independent of genetic polymorphism.
2022-06-30 | GSE183785 | GEO
Project description:Clonal and subclonal evolution is involved in the progression of chronic lymphocytic leukemia (CLL). Evolution can work to select not only genetic mutations, but also epigenetic states. Here we performed a long-term longitudinal DNA methylation profiling study of CLL patients to look for associations of epigenetic evolution to different disease courses. In line with the genetic data, large-scale methylation evolution was not present in any of the evaluated long-term untreated (n = 3) and relapsed (n = 2) patients displaying clonal changes of linear type while 3 of the 5 examined refractory patients featured profound changes in DNA methylation.
2021-03-15 | GSE143411 | GEO
Project description:Arbuscular mycorrhizal (AM) fungi form mutualistic relationships with most land plant species. AM fungi have long been considered as ancient asexuals. Long-term clonal evolution would be remarkable for a eukaryotic lineage and suggests the importance of alternative mechanisms to promote genetic variability facilitating adaptation. Here, we assessed the potential of transposable elements (TEs) for generating genomic diversity. The dynamic expression of TEs during Rhizophagus irregularis spore development suggests ongoing TE activity. We find Mutator-like elements located near genes belonging to highly expanded gene families. Characterising the epigenomic status of R. irregularis provides evidence of DNA methylation and small RNA production occurring at TE loci. Our results support a potential role for TEs in shaping the genome, and roles for DNA methylation and small RNA-mediated silencing in regulating TEs. A well-controlled balance between TE activity and repression may therefore contribute to genome evolution in AM fungi.
2022-02-17 | PXD025245 | Pride
Project description:The evolution of small RNA pathways across the arthropods
| PRJNA386859 | ENA
Project description:Here we characterize an association between disease progression and DNA methylation in Diffuse Large B cell Lymphoma (DLBCL). By profiling genome-wide DNA methylation at single base-pair resolution in thirteen DLBCL diagnosis-relapse sample pairs, we show DLBCL patients exhibit heterogeneous evolution of tumor methylomes during relapse. We identify differentially methylated regulatory elements and determine a relapse–associated methylation signature converging on key pathways such as transforming growth factor beta (TGF-beta) receptor activity. We also observe decreased intra-tumor methylation heterogeneity from diagnosis to relapsed tumor samples. Relapse-free patients display lower intra-tumor methylation heterogeneity at diagnosis compared to relapsed patients in an independent validation cohort. Furthermore, intra-tumor methylation heterogeneity is predictive of time to relapse. Therefore, we propose that epigenomic heterogeneity may support or drive the relapse phenotype and can be used to predict DLBCL relapse. Using ERRBS, we profiled genome-wide DNA methylation patterns of non-relapse DLBCL tumor samples at diagnosis, relaspe DLBCL patient samples at diagnosis and relaspe.
2015-04-14 | E-GEOD-66329 | biostudies-arrayexpress
Project description:Evolution of DNA methylation in Neurospora species
| PRJNA505304 | ENA