Caracterización fenotípica y filogenia molecular de hongos extremófilos
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB38011 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Dieldrin is a legacy pesticide that has multiple modes of action (MOA) that include being an estrogen receptor agonist, GABA receptor antagonist, and a chemical that disrupts mitochondrial function. There is also evidence that dieldrin exposure is significantly associated with an increased risk for neurodegeneration in humans. The objective of this thesis was to clarify the effects of dieldrin in the hypothalamus, the major neuroendocrine region of the brain, in the zebrafish (Danio rerio). Zebrafish were fed pellets containing 0.03, 0.15, or 1.8 µg/g dieldrin for 21 days and a global gene expression analysis was performed to characterize cellular processes and pathways affected by dieldrin.
2016-03-07 | GSE71638 | GEO
Project description:DNA methylation is a conserved epigenetic gene regulation mechanism. DOMAINS REARRANGED METHYLTRANSFERASE (DRM) is a key de novo methyltransferase in plants, but how DRM acts mechanistically is poorly understood. Here, we report the crystal structure of the methyltransferase domain of tobacco DRM (NtDRM) and reveal a molecular basis for its rearranged structure. NtDRM forms a functional homo-dimer critical for catalytic activity. We also show that Arabidopsis DRM2 exists in complex with the siRNA effector ARGONAUTE4 (AGO4) and preferentially methylates one DNA strand, likely the strand acting as the template for non-coding Pol V RNA transcripts. This strand-biased DNA methylation is also positively correlated with strand-biased siRNA accumulation. These data suggest a model in which DRM2 is guided to target loci by AGO4-siRNA and involves base-pairing of associated siRNAs with nascent RNA transcripts. Whole-genome bisulfite sequencing was done for a wildtype line (ecotype Col) as well as various transgenic lines in a drm2 mutant background (ecotype Col). Each transgenic line expressed a version of the DRM2 protein that was either wildtype or carried induced mutations in order to test the function of various domains in the DRM2 protein. Two sets of whole-genome bisulfite were performed (130615 or 131216) and comparisons were mainly done within sets although comparisons can also be done between sets. The drm2 mutant methylome was also analyzed in this study using a previously published whole-genome bisulfite library (GSE39901).
2014-05-27 | E-GEOD-54944 | biostudies-arrayexpress
Project description:The cohesin protein complex is essential for the formation of topologically associating domains (TADs) and chromatin loops on interphase chromosomes. For the loading onto chromosomes, cohesin requires the cohesin loader complex formed by NIPBL and MAU2. Cohesin localizes at enhancers and gene promoters with NIPBL in mammalian cells and forms enhancer-promoter loops. Cornelia de Lange syndrome (CdLS) is a rare, genetically heterogeneous disorder affecting multiple organs and systems during development, caused by mutations in the cohesin loader NIPBL gene (> 60% of patients), as well as in genes encoding cohesin, a chromatin regulator, BRD4, and cohesin-related factors. We also reported CHOPS syndrome that phenotypically overlaps with CdLS and is caused by gene mutations of a super elongation complex (SEC) core component, AFF4. Although these syndromes are associated with transcriptional dysregulation, the underlying mechanism remains unclear. In this study, we provide the first comprehensive analysis of chromosome architectural changes caused by these mutations using cell lines derived from CdLS and CHOPS syndrome patients. In both patient cells, we found a decrease in cohesin, NIPBL, BRD4, and acetylation of lysine 27 on histone H3 (H3K27ac) in most enhancers with enhancer-promoter loop attenuation. In contrast, TADs were maintained in both patient cells. These findings reveal a shared molecular mechanism in these syndromes and highlight unexpected roles for cohesin, cohesin loaders, and the SEC in maintaining the enhancer complexes. These complexes are crucial for recruiting transcriptional regulators, sustaining active histone modifications, and facilitating enhancer-promoter looping.
2025-02-21 | GSE277780 | GEO
Project description:De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own M-bM-^@M-^\coefficientM-bM-^@M-^] of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases. CpG-methylated genomic DNA was enriched using a methyl-DNA immunoprecipitation (mDIP) assay. DNA from the input and bound (enriched) DNA for each sample were labeled and hybridized on the array to define the methylation state of each region.
2014-03-26 | E-GEOD-38142 | biostudies-arrayexpress
Project description: Not available
| S-EPMC11005826 | biostudies-literature
Project description: Not available
| S-EPMC9802440 | biostudies-literature
Project description:De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own “coefficient” of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases.
2014-03-26 | GSE38142 | GEO
Project description:This data serves as an Appendix for the MSc thesis of Logan Jason Smith.
2023-10-15 | MSV000093117 | MassIVE