Conservation, acquisition, and functional impact of sex-biased gene expression in mammalian tissues
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ABSTRACT:
PROVIDER: PRJNA516470 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8474160_1.fastq.gz | Fastqsanger.gz | |||
| SRR8474160_2.fastq.gz | Fastqsanger.gz | |||
| SRR8474170_1.fastq.gz | Fastqsanger.gz | |||
| SRR8474170_2.fastq.gz | Fastqsanger.gz | |||
| SRR8474180_1.fastq.gz | Fastqsanger.gz |
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Project description:Sex differences are widespread in human health and disease, which are frequently modeled in other mammalian species. However, the extent to which molecular sex differences are conserved across both tissues and species remains unclear. We conducted a 12-tissue, five-species survey of sex differences in gene expression using both publicly available (human) and newly generated (cynomolgus macaque, mouse, rat, and dog) RNA sequencing data. In each of the tissues assessed, we identified between 128 and 805 genes with conserved sex-biased expression. However, most sex bias in gene expression (~77%) – both female and male – has arisen since the last common ancestor of boroeutherian mammals, likely facilitated by reduced selective constraint. Evolutionary gains and losses of regulation by sex-biased transcription factors drove a significant fraction (~27%) of lineage-specific changes in sex bias. Our study suggests caution in the use of other species as models of human sex differences, and that similar selective pressures have driven sex-biased gene expression both within and outside the reproductive tract.
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Project description:This study investigates sex-biased gene expression between populations of Atlantic and Pacific salmon lice, Lepeophtheirus salmonis. Two Atlantic L. salmonis populations were previously used for an array study (GSE56024) while a third dataset using Pacific L. salmonis was novel. Using all three populations, a consensus-based, meta-analysis approach was used to identify sex-biased and sex-specific genes.
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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.
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Project description:This study investigates sex-biased gene expression between populations of Atlantic and Pacific salmon lice, Lepeophtheirus salmonis. Two Atlantic L. salmonis populations were previously used for an array study (GSE56024) while a third dataset using Pacific L. salmonis was novel. Using all three populations, a consensus-based, meta-analysis approach was used to identify sex-biased and sex-specific genes. Two separate experiments were conducted, one for Atlantic and one for Pacific salmon lice. As the Atlantic data has been previously published for other comparisons (GSE56024), only the Pacific data is uploaded here. Lice from three populations (2 in the Atlantic and 1 in the Pacific) were collected for in vitro bioassay analysis using emamectin benzoate. After 24hrs, lice were collected as per treatment protocol below. Males and females from all populations were compared separately before forming a consensus probe list of sex-biased genes concordantly expressed across all three populations. Please note that each raw data file contains three or four 'block' data and each block data correspond to individual sample raw data. Therefore, each raw data file contains raw data for 3-4 samples (as indicated in the description field).
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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.
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