LPS stimulation reveals male and female dimorphism in human iPSC-derived macrophages
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE328566 | GEO | 2026/08/01
REPOSITORIES: GEO
Similar Datasets
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. Profiling of expression levels in Nasonia vitripennis and Nasonia giraulti adult male and female samples using Illumina RNA-seq
2015-06-08 | E-GEOD-61156 | biostudies-arrayexpress
Project description:LPS stimulation reveals male and female dimorphism in human iPSC-derived macrophages
| PRJNA1455650 | ENA
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.
2015-06-08 | GSE61156 | 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.
2015-06-08 | GSE61158 | 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:In the present study we used a proteomic approach to identify and quantify protein abundance differences between male and female zebrafish heart to explore, at the molecular level, any possible sex-biased differences in the heart as the central part of the cardiovascular system for this model organism. The results from the study provide a novel and wide proteome resource, which could be further used to study the role of the identified proteins in the cardiovascular system in both sexes. Furthermore, we hope that this study may open a new window towards the development of sex and gender-based drugs and it establishes sex as a factor to be considered when designing toxicological experiments.
2021-06-28 | PXD023506 | Pride
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: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: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:Sex differences in hepatocellular carcinoma (HCC) development are regulated by sex and non-sex chromosomes, sex hormones, and environmental factors. We previously reported that Ncoa5+/- mice develop HCC in a male-biased manner. Here we show that NCOA5 expression was reduced in male patient HCCs while the expression of an NCOA5-interacting tumor suppressor, TIP30, was lower in female HCCs. Tip30 heterozygous deletion did not change HCC incidence in Ncoa5+/- male mice but dramatically increased HCC incidence in Ncoa5+/- female mice, accompanied by hepatic hyperpolarization-activated cyclic nucleotide-gated cation channel 3 (HCN3) overexpression. HCN3 overexpression cooperated with MYC to promote mouse HCC development, whereas Hcn3 knockout preferentially hindered HCC development in female mice. Furthermore, HCN3 amplification and overexpression occurred in human HCCs and correlated with a poorer prognosis of patients in a female-biased manner. Our results suggest that TIP30 and NCOA5 protect against female liver oncogenesis and that HCN3 is a female-biased HCC driver.
2023-08-29 | GSE228531 | GEO