Ranidae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA478189 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Frogs are an ecologically diverse and phylogenetically ancient group of anuran amphibians that include important vertebrate cell and developmental model systems, notably the genus Xenopus. Here we report a high-quality reference genome sequence for the western clawed frog, Xenopus tropicalis, along with draft chromosome-scale sequences of three distantly related emerging model frog species, Eleutherodactylus coqui, Engystomops pustulosus and Hymenochirus boettgeri. Frog chromosomes have remained remarkably stable since the Mesozoic Era, with limited Robertsonian (i.e., centric) translocations and end-to-end fusions found among the smaller chromosomes. Conservation of synteny includes conservation of centromere locations, marked by centromeric tandem repeats associated with Cenp-a binding, surrounded by pericentromeric LINE/L1 elements. We explored chromosome structure across frogs, using a dense meiotic linkage map for X. tropicalis and chromatin conformation capture (Hi-C) data for all species. Abundant satellite repeats occupy the unusually long (~20 megabase) terminal regions of each chromosome that coincide with high rates of recombination. Both embryonic and differentiated cells show reproducible association of centromeric chromatin, and of telomeres, reflecting a Rabl-like configuration. Our comparative analyses reveal 13 conserved ancestral anuran chromosomes from which contemporary frog genomes were constructed.
2022-03-30 | GSE199671 | GEO
Project description:Sex differences in the brain as they relate to health and disease are often overlooked in experimental models. Many neurological disorders, like Alzheimer’s disease (AD), multiple sclerosis (MS), and autism, differ in prevalence between males and females. Sex differences originate either from differential gene expression on sex chromosomes or from hormonal differences, either directly or indirectly. To disentangle the relative contributions of genetic sex (XX v. XY) and gonadal sex (ovaries v. testes) to the regulation of hippocampal sex effects, we use the “sex-reversal” Four Core Genotype (FCG) mouse model which uncouples sex chromosome complement from gonadal sex. Transcriptomic and epigenomic analyses of hippocampal RNA and DNA from ∼12 month old FCG mice, reveals differential regulatory effects of sex chromosome content and gonadal sex on X- versus autosome-encoded gene expression and DNA modification patterns. Gene expression and DNA methylation patterns on the X chromosome were driven primarily by sex chromosome content, not gonadal sex. The majority of DNA methylation changes involved hypermethylation in the XX genotypes (as compared to XY) in the CpG context, with the largest differences in CpG islands, promoters, and CTCF binding sites. Autosomal gene expression and DNA modifications demonstrated regulation by sex chromosome complement and gonadal sex. These data demonstrate the importance of sex chromosomes themselves, independent of hormonal status, in regulating hippocampal sex effects. Future studies will need to further interrogate specific CNS cell types, identify the mechanisms by which sex chromosome regulate autosomes, and differentiate organizational from activational hormonal effects.
2022-01-31 | GSE184098 | GEO
Project description:Sex differences in the brain as they relate to health and disease are often overlooked in experimental models. Many neurological disorders, like Alzheimer’s disease (AD), multiple sclerosis (MS), and autism, differ in prevalence between males and females. Sex differences originate either from differential gene expression on sex chromosomes or from hormonal differences, either directly or indirectly. To disentangle the relative contributions of genetic sex (XX v. XY) and gonadal sex (ovaries v. testes) to the regulation of hippocampal sex effects, we use the “sex-reversal” Four Core Genotype (FCG) mouse model which uncouples sex chromosome complement from gonadal sex. Transcriptomic and epigenomic analyses of hippocampal RNA and DNA from ∼12 month old FCG mice, reveals differential regulatory effects of sex chromosome content and gonadal sex on X- versus autosome-encoded gene expression and DNA modification patterns. Gene expression and DNA methylation patterns on the X chromosome were driven primarily by sex chromosome content, not gonadal sex. The majority of DNA methylation changes involved hypermethylation in the XX genotypes (as compared to XY) in the CpG context, with the largest differences in CpG islands, promoters, and CTCF binding sites. Autosomal gene expression and DNA modifications demonstrated regulation by sex chromosome complement and gonadal sex. These data demonstrate the importance of sex chromosomes themselves, independent of hormonal status, in regulating hippocampal sex effects. Future studies will need to further interrogate specific CNS cell types, identify the mechanisms by which sex chromosome regulate autosomes, and differentiate organizational from activational hormonal effects.
2022-01-31 | GSE184013 | GEO
Project description:Sex biases in the genome-wide distribution of DNA methylation and gene expression levels are some of the manifestations of sexual dimorphism in mammals. To advance our understanding of the mechanisms that contribute to sex biases in DNA methylation and gene expression, we conducted whole genome bisulfite sequencing (WGBS) as well as RNA-seq on liver samples from mice with different combinations of sex phenotype and sex-chromosome complement. We compared groups of animals with different sex phenotypes, but the same genetic sexes, and vice versa, same sex phenotypes, but different sex-chromosome complements. We also compared sex-biased DNA methylation in mouse and human livers. Our data show that sex phenotype, X-chromosome dosage, and the presence of Y chromosome shape the differences in DNA methylation between males and females. We also demonstrate that sex bias in autosomal methylation is associated with sex bias in gene expression, whereas X-chromosome dosage-dependent methylation differences are not, as expected for a dosage-compensation mechanism. Furthermore, we find partial conservation between the repertoires of mouse and human genes that are associated with sex-biased methylation, an indication that gene function is likely to be an important factor in this phenomenon.
2022-11-14 | GSE217666 | GEO
Project description:The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages.
2016-04-06 | GSE77794 | GEO
Project description:Biological sex determination of human remains by means of a minimally destructive surface acid etch of tooth enamel and subsequent identification of sex chromosome linked isoforms of Amelogenin– an enamel-forming protein - by nano-liquid chromatography mass spectrometry(nanoLC-MS).
2017-12-12 | PXD007856 | Pride
Project description:Along with the prevalence of edible frog farming in China, the outbreak of a deadly infectious frog diseased, called frog meningitis (or cataracts and torticollis), has increased in frequency and geographical range dramatically. More than 10 bacterial species, belonging to 8 genera, has been reported as its potential pathogens. Diseased frogs typically manifest as torticollis, cataracts, edema and finally death, resulting in huge economic loss. Currently, the pathogenesis of this disease has not been investigated systematically. Here, we summarized the pathological stages of infected black-spotted frogs (Pelophylax nigromaculata) in Sichuan province according to their symptoms, typically progressing of pathological stage with only torticollis to stage with both torticollis and cataracts. On the basis, we analyzed the pathogenesis by a combination of comparative environmental analysis, microbiomics and transcriptomics. Results showed that more severely infected frog ponds tended to have lower water alkalinity. Elizabethkingia miricola was the only bacteria, whose abundance was positively correlated with the disease degree, and it has absolute dominance in the eyeball and brain of some torticollis-cataracts frogs. E. miricola and several other bacterial species, which belonged to pathogenic genera of meningitis, might be constitutively existed in the resident microbiome in frogs or their environment. Activations of infectious processes and immune responses related pathways were the major difference between health and diseased frogs at transcriptional level. Despite transcriptional activation of immunoglobulins was observed in both torticollis-only and torticollis-cataracts frogs, transcriptional activation of innate immune system (including MHC, toll-like receptor, and cathelicidins) in brain, inflammation system (including interleukins and receptors) in brain, and acute phase proteins (including transferrins and fibrinogens) in both liver and brain was only observed in torticollis-cataracts frogs. Activation of inflammation and the resulting higher vascular permeability in torticollis-cataracts frogs could explain the severe brain infection, cooccurrence of torticollis and cataracts, and systemic edema in torticollis-cataracts frogs. In addition, meningitis could also result in reduction in energy production in liver, and this was more severe in torticollis-cataracts frogs. In conclusion, our results suggested environment might have a role in susceptibility of frog meningitis. E. miricola was the most likely pathogen of meningitis of black-spotted frogs in Sichuan. Refer to the pathogenesis of human meningitis, excessive inflammation likely played a critical role in the progress of frog meningitis, and its resulted sepsis and organ failure might be the direct cause of infected frogs.
2020-06-05 | GSE132282 | GEO