Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731608 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Whole brain gene expression profiling for Julidochromis transcriptus male vs. female and Julidochromis marlieri male vs female to identify sex-role biased and sex biased gene expression in these species that exhibit conventional and reversed sex-biased behavior respectively.
2010-07-24 | GSE23094 | GEO
Project description:Sexual dimorphism depends on sex-biased gene expression, but the contributions of microRNAs (miRNAs) have not been globally assessed. We therefore produced an extensive small RNA sequencing dataset to analyse male and female miRNA expression profiles in mouse, opossum and chicken. Our analyses uncovered numerous cases of somatic sex-biased miRNA expression, especially in the mouse heart and liver. Sex-biased expression is explained by miRNA-specific regulation, including sex-biased chromatin accessibility at promoters, rather than piggybacking of intronic miRNAs on sex-biased protein-coding genes. In mouse, but not opossum and chicken, sex bias is coordinated across tissues such that autosomal testis-biased miRNAs tend to be somatically male-biased, whereas autosomal ovary-biased miRNAs are female-biased, possibly due to broad hormonal control. In chicken, which has a Z/W sex chromosome system, expression output of genes on the Z chromosome is expected to be male-biased, since there is no global dosage compensation mechanism that restores expression in ZW females after almost all genes on the W chromosome decayed. Nevertheless, we found that the dominant liver miRNA, miR-122-5p, is Z-linked but expressed in an unbiased manner, due to the unusual retention of a W-linked copy. Another Z-linked miRNA, the male-biased miR-2954-3p, shows conserved preference for dosage-sensitive genes on the Z chromosome, based on computational and experimental data from chicken and zebra finch, and acts to equalise male-to-female expression ratios of its targets. Unexpectedly, our findings thus establish miRNA regulation as a novel gene-specific dosage compensation mechanism.
2017-11-01 | GSE102062 | GEO
Project description:Here we map six chromatin modifications -- H3K4me1, H3K4me3, H3K27ac, H3K36me3, H3K9me3, and H3K27me3 -- genome-wide in male and female mouse liver in order to identify histone modifications that characterize sex-biased genes and sex-biased DNase hypersensitive sites and their regulation by plasma growth hormone (GH) profiles, which are sexually dimorphic. We find distinct mechanisms of regulation in male liver and female liver: sex-dependent K27me3-mediated repression is an important mechanism of repression of female-biased, but not of male-biased, genes, and a sex-dependent K4me1 distribution, suggesting nucleosome repositioning by pioneer factors, is observed at male-biased, but not female-biased, regulatory sites. STAT5-mediated activation is most strongly associated with sex-biased chromatin modifications, while BCL6-mediated repression primarily occurs in association with sex-independent chromatin modifications, both at binding sites and at target genes. These samples are part of a study on chromatin states in male and female mouse and their role in sex-biased liver gene expression (A Sugathan and DJ Waxman (2013) Molec Cell Biol).
2013-07-03 | GSE44571 | GEO
Project description:The extraordinary range in the degree of sexual dimorphism (SD) among animal species is widely perceived to be caused in part by differences in patterns of sexual selection, but sex-specific adaptations and sex chromosome differences also play a role. Studies in insects have discovered a substantial number of sex-biased genes, but little is known about the epigenetic basis of SD. The degree and genome-wide distribution of sex-biased expression become interesting questions in hymenoptera species with haplodiploid sex-determination. To study the genetic and epigenetic architecture of SD and understand the conservation and evolution of sex-biased expression in a haplodiploid system that lacks sex chromosomes, we performed RNA-seq and whole-genome bisulfite sequencing in female and male adult samples of two parasitoid wasp species, Nasonia vitripennis and Nasonia giraulti. More than 75% of the expressed genes displayed significantly sex-biased expression. Both the number and the degree of sex-biased genes are higher than insects like Drosophila melanogaster, which have sex-chromosome mediated sex determination. Females from the two Nasonia species have far more similar expression profiles than does the contrast between the two sexes within either species. Interestingly, the extremely male- and female-biased genes are enriched for totally different functional categories: male-biased genes are highly enriched for key enzymes in sex-pheromone synthesis; female-biased genes are enriched for nuclear-located genes that are responsible for epigenetic regulation of gene expression. Unlike gene expression profiles, DNA methylomes are more similar within species, and no stable differentially methylated genes have been found between the two sexes, suggesting that DNA methylation is not directly responsible for the molecular basis of SD. However, methylation status does influence sex-biased expression: 80% of female-biased genes are methylated, which is more than two-fold higher than the genome average (30%); almost all male-biased and sex-specific genes are non-methylated, which is consistent with the fact that methylated genes have house-keeping functions and a broader expression breadth. Evolutionarily, male-biased genes have greater sequence divergence between the two species, and they are more likely to have a functional paralog in the Nasonia genome. Sex-specific genes have significantly higher non-synonymous substitution rates and dN/dS ratios. In addition, local clusters of sex-biased genes in the genome may have epigenetic properties similar to the sex chromosome. In summary, Nasonia accomplish a striking degree of sex-differential expression through a difference in ploidy along with associated differences in methylations status. Whole-genome bisulfite sequencing of 24-hour adult whole body samples of Nasonia vitripennis and Nasonia giraulti using Iilumina sequencing.
2015-06-08 | E-GEOD-61158 | biostudies-arrayexpress
Project description:Investigatation into how genes with sex-differential expression profiles are distributed among the chromosomes in Drosophila. Assayed the expression of 14,142 predicted transcripts in competitive hybridizations and found a dramatic underrepresentation of X-chromosome genes showing high relative expression in male. This is the first report of sex-biased expression of the full (predicted) genome. Findings indicate that there is significant sex-biased expression, especially in gonads. Genes showing sex-biased gene expression profiles are likely to have sex-biased functions. Keywords: other
2003-06-02 | GSE442 | GEO
Project description:Sex differences in gene expression throughout development are poorly understood, especially sex-specific expression of micro RNAs. However these patterns of gene expression could have important implications in our understanding of the underlying mechanics of sex differentiation and sexual conflict. We extract mRNA and miRNA from male and female Drosophila melanogaster from three developmental timepoints, third larval instar, pupae and adults, and examine gene expression using microarrays. We found a large number of sex-biased mRNA transcripts at each stage of development, whereas sex-biased miRNA expression was low in larvae and pupae and more prevalent in adults.
2014-05-07 | GSE57321 | GEO
Project description:Here we map six chromatin modifications -- H3K4me1, H3K4me3, H3K27ac, H3K36me3, H3K9me3, and H3K27me3 -- genome-wide in male and female mouse liver in order to identify histone modifications that characterize sex-biased genes and sex-biased DNase hypersensitive sites and their regulation by plasma growth hormone (GH) profiles, which are sexually dimorphic. We find distinct mechanisms of regulation in male liver and female liver: sex-dependent K27me3-mediated repression is an important mechanism of repression of female-biased, but not of male-biased, genes, and a sex-dependent K4me1 distribution, suggesting nucleosome repositioning by pioneer factors, is observed at male-biased, but not female-biased, regulatory sites. STAT5-mediated activation is most strongly associated with sex-biased chromatin modifications, while BCL6-mediated repression primarily occurs in association with sex-independent chromatin modifications, both at binding sites and at target genes. These samples are part of a study on chromatin states in male and female mouse and their role in sex-biased liver gene expression (A Sugathan and DJ Waxman (2013) Molec Cell Biol). Examination of six different histone modifications in male and female mouse liver.
2013-07-03 | E-GEOD-44571 | biostudies-arrayexpress
Project description:Sex-dependent pituitary growth hormone (GH) secretory patterns determine the sex-biased expression of >1,000 genes in mouse and rat liver, affecting lipid and drug metabolism, inflammation and disease. A fundamental biological question is how robust differential expression can be achieved for hundreds of sex-biased genes simply based on the GH input signal pattern: pulsatile GH stimulation in males vs. near-continuous GH exposure in females. STAT5 is an essential transcriptional mediator of the sex-dependent effects of GH in the liver, but the mechanisms that underlie its sex-dependent actions are obscure. Here we elucidate the dynamic, sex-dependent binding of STAT5 and the GH/STAT5-regulated repressor BCL6 to mouse liver chromatin, revealing the counteractive interplay between these two regulators of liver sex-specificity. Our findings establish a close correlation between sex-dependent STAT5 binding and sex-biased target gene expression. Moreover, sex-dependent STAT5 binding correlated positively with sex-biased DNase hypersensitivity and H3-K4me1 and H3-K4me3 (activating) marks, correlated negatively with sex-biased H3-K27me3 (repressive) marks, and was associated with sex-differentially enriched motifs for HNF6/CDP factors. Importantly, BCL6 binding was preferentially associated with repression of female-biased STAT5 targets in male liver. Furthermore, BCL6 and STAT5 common targets but not BCL6 unique targets showed strong enrichment for lipid and drug metabolism. These findings provide a comprehensive, genome-wide view of the mechanisms whereby these two GH-regulated transcription factors establish and maintain sex differences affecting liver physiology and disease. The approaches used here to characterize sex-dependent STAT5 and BCL6 binding can be applied to other condition-specific regulatory factors and binding sites and their interplay with co-operative chromatin-binding factors.
2011-12-18 | GSE31578 | GEO