Sex-biased gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE442 | GEO | 2003/06/02
SECONDARY ACCESSION(S): PRJNA85027
REPOSITORIES: GEO
Similar Datasets
Project description:Investigation of sex-biased expression across species have relied on measurements from whole flies which sample the extensive expression differences found in the germline and gonads of females and males. We wanted to examine genes with sex-biased expression in a somatic tissue to analyze patterns of genes with sex-biased expression in the context of a tissue more phenotypically similar between females and males. We used a Nimblegen microarray designed for Drosophila melanogaster and two custom micoarrays designed for D. pseudoobscura and D. mojavensis to survey gene expression differences in heads of females and males.
2010-07-30 | GSE23309 | GEO
Project description:Investigation of sex-biased expression across species have relied on measurements from whole flies which sample the extensive expression differences found in the germline and gonads of females and males. We wanted to examine genes with sex-biased expression in a somatic tissue to analyze patterns of genes with sex-biased expression in the context of a tissue more phenotypically similar between females and males. We used a Nimblegen microarray designed for Drosophila melanogaster and two custom micoarrays designed for D. pseudoobscura and D. mojavensis to survey gene expression differences in heads of females and males. PolyA+ mRNA was isolated in quadruplicate from dissected heads of 8 day old adult females and males. Female and male mRNA were labeled with Cy3 or Cy5 dyes separately and co-hybridized to species-specific microarrays. We analyzed a total of 24 channels of data.
2010-07-30 | E-GEOD-23309 | biostudies-arrayexpress
Project description:Sex-differences in human liver gene expression were characterized on a genome-wide scale using a large liver sample collection, allowing for detection of small expression differences with high statistical power. 1,249 sex-biased genes were identified, 70% showing higher expression in females. Chromosomal bias was apparent, with female-biased genes enriched on chrX and male-biased genes enriched on chrY and chr19, where 11 male-biased zinc-finger KRAB-repressor domain genes are distributed in six clusters. Top biological functions and diseases significantly enriched in sex-biased genes include transcription, chromatin organization and modification, sexual reproduction, lipid metabolism and cardiovascular disease. Notably, sex-biased genes are enriched at loci associated with polygenic dyslipidemia and coronary artery disease in genome-wide association studies. Moreover, of the 8 sex-biased genes at these loci, 4 have been directly linked to monogenic disorders of lipid metabolism and show an expression profile in females (elevated expression of ABCA1, APOA5 and LDLR; reduced expression of LIPC) that is consistent with the lower female risk of coronary artery disease. Female-biased expression was also observed for CYP7A1, which is activated by drugs used to treat hypercholesterolemia. Several sex-biased drug-metabolizing enzyme genes were identified, including members of the CYP, UGT, GPX and ALDH families. Half of 879 mouse orthologs, including many genes of lipid metabolism and homeostasis, show growth hormone-regulated sex-biased expression in mouse liver, suggesting growth hormone might play a similar regulatory role in human liver. Finally, the evolutionary rate of protein-coding regions for human-mouse orthologs, revealed by dN/dS ratio, is significantly higher for genes showing the same sex-bias in both species than for non-sex-biased genes. These findings establish that human hepatic sex differences are widespread and affect diverse cell metabolic processes, and may help explain sex differences in lipid profiles associated with sex differential risk of coronary artery disease.
2011-08-17 | GSE23766 | GEO
Project description:Although not all sex-dependent gene expression is adaptive, it is likely an important genomic mechanism that allows each sex to independently adapt to environmental changes. Among Drosophila species, sex-biased genes display remarkably consistent evolutionary patterns; male-biased genes evolve faster than unbiased genes in both coding sequence and expression level, suggesting sex-differences in selection through time. However, comparatively little is known of the evolutionary process shaping sex-biased expression within species. Latitudinal clines offer an opportunity to examine how changes in key ecological parameters also influence sex-specific selection and the evolution of sex-biased gene expression. We assayed male and female gene expression in Drosophila serrata along a latitudinal gradient in eastern Australia spanning most of its endemic distribution. Analysis of 11,631 genes across eight populations revealed strong sex differences in the frequency, mode, and strength of divergence. Divergence was far stronger in males than females and while latitudinal clines were evident in both sexes, male divergence was often population-specific, suggesting responses to localized selection pressures that do not covary predictably with latitude. While divergence was enriched for male-biased genes, there was no overrepresentation of X-linked genes in males. By contrast, X-linked divergence was elevated in females, especially for female biased genes. Many genes that diverged in D. serrata have homologs also showing latitudinal divergence in D. simulans and D. melanogaster on other continents, likely indicating parallel adaptation in these distantly related species. Our results suggest that sex differences in selection play an important role in shaping the evolution of gene expression over macro- and micro-ecological spatial scales.
2017-01-04 | GSE90733 | GEO
Project description:Mammalian sex differences are determined by the X and Y chromosomes. Ancestral homologous genes on the sex chromosomes, termed X-Y gene pairs, have been predicted to drive sex differences. However, among the five X-Y gene pairs conserved across eutherians, which pairs drive sex-biased gene expression have remained undefined. Here, we investigate the roles of the X-Y gene pair Kdm5c-Kdm5d in regulating sex-biased gene expression independently of sex hormones using pluripotent mouse embryonic stem cells (ESCs) as a model. Wild-type (WT) XX female and WT XY male ESCs significantly differ in the expression of approximately 4% of all expressed genes, classified as female- or male-biased. Loss of Kdm5c in female ESCs results in the downregulation of female-biased genes. In contrast, loss of either Kdm5c or Kdm5d in male ESCs results in the upregulation of female-biased genes and downregulation of male-biased genes, effectively neutralizing sex-biased gene expression. In male ESCs, most sex-biased genes change in expression in a similar direction upon loss of Kdm5c or Kdm5d. However, Kdm5c loss dysregulates a greater number of sex-biased genes relative to Kdm5d loss in male ESCs. Remarkably, in female ESCs ectopic Kdm5d expression is sufficient to drive a sex-biased gene expression pattern similar to that of WT male ESCs. Taken together, these results establish Kdm5c-Kdm5d as a critical X-Y gene pair in driving sex-biased gene expression in pluripotent cells.
2024-12-13 | GSE277494 | GEO
Project description:Purpose: Accurate identification of sex-biased genes requires precise measurement of gene expression levels in gonads. This study is designed to provide such data for various Drosophila species to enhance studies of sex-biased gene expression and evolution across the genus. Methods: Virgin flies were collected and aged 6-10 days before dissecting 2-3 replicates of testes or ovaries. Total RNA was extracted using the Arcturus® PicoPure® kit . Illumina® TruSeq® RNA library kits were used to poly-A+ select and reverse-transcribe mRNA, shear cDNA into ~120 bp fragments, and produce libraries for 1x50 bp sequencing on an Illumina GAIIx or HiSeq2000. Illumina®’s Real Time Analysis v1.13 module processed images, called bases, and provided base qualities. Reads were mapped to the current reference genomes using Bowtie v2.1.0 (Langmead and Salzberg, 2012, Nat Meth) with default settings. Differentially expressed genes were detected using Cufflinks v 2.1.0 (Trapnell et al., 2010, Nat Biotech; default settings) or edgeR (Robinson et al., 2010, Bioinformatics; full-quantile GC-content normalization and full-quantile between-sample normalization). Genes were called differentially expressed at a Benjamini-Hochberg false discovery rate of 0.01. Results: Thousands of male- and female-biased genes were detected for each species using both DE detection methods. These results provide a significant improvement in sensitivity of sex-biased gene detection relative to using whole-body RNA-sequencing data. These data provide a foundation for accurate identification of sex-biased genes throughout the Drosophila genus.
2013-11-04 | GSE52058 | GEO
Project description:Avian sex is determined by various factors, such as the dosage of DMRT1 and cell-autonomous mechanisms. While the sex-determination mechanism in gonads is well analyzed, the mechanism in germ cells remains unclear. In this study, we explored the gene expression profiles of male and female primordial germ cells (PGCs) during embryogenesis in chickens to predict the mechanism of sex-determination. Male and female PGCs were isolated from blood and gonads with a purity > 96% using flow cytometry and analyzed using RNA-seq. Prior to settlement in the gonads, female circulating PGCs (cPGCs) obtained from blood displayed sex-biased expression. Gonadal PGCs (gPGCs) also displayed sex-biased expression, and the number of female-biased genes detected was higher than male-biased genes. The female-biased genes in gPGCs were enriched in some metabolic processes. To reveal the mechanisms underlying the transcriptional regulation of female-biased genes in gPGCs, we performed stimulation tests. Stimulation with retinoic acid against cultured gPGCs derived from male embryos resulted in the upregulation of several female-biased genes. Overall, our results suggest that sex determination of avian PGCs possess aspects of both cell-autonomous and somatic cell regulation. Moreover, it appears that sex determination occurs earlier in females than in males.
2022-02-24 | GSE188689 | GEO
Project description:Purpose: Accurate identification of sex-biased genes requires precise measurement of gene expression levels in gonads. This study is designed to provide such data for various Drosophila species to enhance studies of sex-biased gene expression and evolution across the genus. Methods: Virgin flies were collected and aged 6-10 days before dissecting 2-3 replicates of testes or ovaries. Total RNA was extracted using the Arcturus® PicoPure® kit . Illumina® TruSeq® RNA library kits were used to poly-A+ select and reverse-transcribe mRNA, shear cDNA into ~120 bp fragments, and produce libraries for 1x50 bp sequencing on an Illumina GAIIx or HiSeq2000. Illumina®’s Real Time Analysis v1.13 module processed images, called bases, and provided base qualities. Reads were mapped to the current reference genomes using Bowtie v2.1.0 (Langmead and Salzberg, 2012, Nat Meth) with default settings. Differentially expressed genes were detected using Cufflinks v 2.1.0 (Trapnell et al., 2010, Nat Biotech; default settings) or edgeR (Robinson et al., 2010, Bioinformatics; full-quantile GC-content normalization and full-quantile between-sample normalization). Genes were called differentially expressed at a Benjamini-Hochberg false discovery rate of 0.01. Results: Thousands of male- and female-biased genes were detected for each species using both DE detection methods. These results provide a significant improvement in sensitivity of sex-biased gene detection relative to using whole-body RNA-sequencing data. These data provide a foundation for accurate identification of sex-biased genes throughout the Drosophila genus. Testis and ovary samples from Drosophila species were sequenced 1 x 50 bp in duplicate from 6-10 day old virgin, Wolbachia-free adult flies on an Illumina GAIIx or HiSeq2000.
2013-11-04 | E-GEOD-52058 | biostudies-arrayexpress
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:Sex-differences in human liver gene expression were characterized on a genome-wide scale using a large liver sample collection, allowing for detection of small expression differences with high statistical power. 1,249 sex-biased genes were identified, 70% showing higher expression in females. Chromosomal bias was apparent, with female-biased genes enriched on chrX and male-biased genes enriched on chrY and chr19, where 11 male-biased zinc-finger KRAB-repressor domain genes are distributed in six clusters. Top biological functions and diseases significantly enriched in sex-biased genes include transcription, chromatin organization and modification, sexual reproduction, lipid metabolism and cardiovascular disease. Notably, sex-biased genes are enriched at loci associated with polygenic dyslipidemia and coronary artery disease in genome-wide association studies. Moreover, of the 8 sex-biased genes at these loci, 4 have been directly linked to monogenic disorders of lipid metabolism and show an expression profile in females (elevated expression of ABCA1, APOA5 and LDLR; reduced expression of LIPC) that is consistent with the lower female risk of coronary artery disease. Female-biased expression was also observed for CYP7A1, which is activated by drugs used to treat hypercholesterolemia. Several sex-biased drug-metabolizing enzyme genes were identified, including members of the CYP, UGT, GPX and ALDH families. Half of 879 mouse orthologs, including many genes of lipid metabolism and homeostasis, show growth hormone-regulated sex-biased expression in mouse liver, suggesting growth hormone might play a similar regulatory role in human liver. Finally, the evolutionary rate of protein-coding regions for human-mouse orthologs, revealed by dN/dS ratio, is significantly higher for genes showing the same sex-bias in both species than for non-sex-biased genes. These findings establish that human hepatic sex differences are widespread and affect diverse cell metabolic processes, and may help explain sex differences in lipid profiles associated with sex differential risk of coronary artery disease. A first set of randomized liver RNA pools (WS9) was generated by randomly distributing 112 male and 112 female liver RNA samples into 8 pools comprised of 14 male liver samples (pools M1 to M8), and 8 pools of 14 female liver samples each (pools F1 to F8). A second set of 16 pools (WS10) was prepared from the same set of 224 liver samples in the same way (pools M9 to M16 and F9 to F16). The 16 liver RNA pools of each sex were used in a total of 16 male vs. female two-color hybridization microarrays by pairing pool M1 and pool F1, pool M2 with pool F2, etc. Fluorescent labeling of RNA and hybridization of the Alexa 555-labeled and Alexa 647-labeled amplified RNA samples to Agilent Whole Human Genome oligonucleotide microarrays (4 x 44K format; Agilent Technology, Palo Alto, CA; catalog # G4112F) were carried out, with dye swaps to eliminate dye bias.
2011-08-16 | E-GEOD-23766 | biostudies-arrayexpress