Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of sex chromosome complement in autosomal gene expression

ABSTRACT: It has generally been assumed that most differences between males and females are due to developmental and hormonal differences between the sexes. Here we investigate the contribution of sex chromosomal complement to such sexual dimorphisms. These genome-wide transcription profiling showed that the expression of hundreds of autosomal genes was sensitive to sex chromosome complement, rather than gender. The existence of such differences between males and females holds important implications for understanding sexual dimorphisms in physiology and disease hitherto attributed solely to gender or hormonal effects. Thymic total RNA was isolated from 7-8 week old mice, with 3 biological replicates for each of four genotypes with different sex chromosome complements

ORGANISM(S): Mus musculus

SUBMITTER: Patrick Wijchers

PROVIDER: E-GEOD-21822 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Sexual dimorphism in mammalian autosomal gene regulation is determined not only by Sry but by sex chromosome complement as well.

Wijchers Patrick J PJ Yandim Cihangir C Panousopoulou Eleni E Ahmad Mushfika M Harker Nicky N Saveliev Alexander A Burgoyne Paul S PS Festenstein Richard R

Developmental cell 20100901 3

Differences between males and females are normally attributed to developmental and hormonal differences between the sexes. Here, we demonstrate differences between males and females in gene silencing using a heterochromatin-sensitive reporter gene. Using "sex-reversal" mouse models with varying sex chromosome complements, we found that this differential gene silencing was determined by X chromosome complement, rather than sex. Genome-wide transcription profiling showed that the expression of hun ...[more]

PMID: 20833369

Similar Datasets

Role of sex chromosome complement in autosomal gene expression

Project description:It has generally been assumed that most differences between males and females are due to developmental and hormonal differences between the sexes. Here we investigate the contribution of sex chromosomal complement to such sexual dimorphisms. These genome-wide transcription profiling showed that the expression of hundreds of autosomal genes was sensitive to sex chromosome complement, rather than gender. The existence of such differences between males and females holds important implications for understanding sexual dimorphisms in physiology and disease hitherto attributed solely to gender or hormonal effects.

2010-10-02 | GSE21822 | GEO

Spenito-dependent metabolic sexual dimorphism intrinsic to fat storage cells

Project description:Metabolism in males and females is distinct. Differences are usually linked to sexual reproduction, with circulating signals (e.g. hormones) playing major roles. By contrast, sex differences prior to sexual maturity and intrinsic to individual metabolic tissues are less understood. We analyzed Drosophila melanogaster larvae and find that males store more fat than females, the opposite of the sexual dimorphism in adults. We show that metabolic differences are intrinsic to the major fat storage tissue, including many differences in the expression of metabolic genes. Our previous work identified fat storage roles for Spenito (Nito), a conserved RNA-binding protein and regulator of sex determination. Nito knockdown specifically in the fat storage tissue abolished fat differences between males and females. We further show that Nito is required for sex-specific expression of the master regulator of sex determination, Sex-lethal (Sxl). “Feminization” of fat storage cells via tissue-specific overexpression of a Sxl target gene made larvae lean, reduced the fat differences between males and females, and induced female-like metabolic gene expression. Altogether, this study supports a model in which Nito autonomously controls sexual dimorphisms and differential expression of metabolic genes in fat cells in part through its regulation of the sex determination pathway.

2023-04-25 | GSE229991 | GEO

Adult sex change leads to extensive forebrain reorganization in clownfish

Project description:Sex differences in the brain have been demonstrated in all major vertebrate lineages but are not well understood at a molecular and cellular level. Sex-changing fishes provide a unique opportunity to uncover mechanisms underlying sexual differentiation of the brain and regulation of sexual phenotypes. Sex change requires the complete transformation of the gonads and behaviors, which in turn require transformation of sexually-differentiated control mechanisms in the brain. However, detailed molecular and cellular profiling of sex differences in the brains of sex-changing fish is lacking. In this study we applied single nucleus RNA-sequencing (snRNA-seq) to generate the first atlas of sex differences in preoptic area (POA) and telencephalon of the model anemonefish Amphiprion ocellaris. We uncovered remarkably widespread sex differences in cell-type abundance and cell-type transcriptome. The most prominent difference was observed in the dorsal medial telencephalon where females displayed more than twice as many glutamatergic neurons as males and more than 400 differentially expressed genes consistent with immature neuronal development in males relative to females. These results provide an unparalleled level of depth to our understanding of sexual differentiation in the brain of a sex-changing fish, and richly characterizes numerous specific sexual dimorphisms that must develop during sex change.

2024-08-16 | GSE246731 | GEO

Emergence of sex-specific transcriptomes in a sexually-dimorphic brain nucleus

Project description:Sexual dimorphisms in the brain give rise to sex differences in physiology and behavior, yet we have limited understanding of the transcriptomic changes underlying their development. We evaluated developmental transcriptome dynamics for one of the most extreme neuroanatomical sexual dimorphisms in vertebrates - the songbird robust nucleus of the arcopallium (RA). RA is the telencephalic motor output nucleus of the song system. It grows monomorphically for the first few weeks posthatch, then continues growing in males but regresses in females, becoming 5-7 times larger in males. We quantified RA gene expression from monomorphic and dimorphic stages of development in both sexes. Mirroring the morphology, male and female transcriptomes initially resembled one other, then diverged markedly. Thousands of genes showed developmental regulation, corresponding to highly sex-specific biological processes. Males showed enrichments for neuronal growth and morphogenesis, synapse organization, metabolism, and voltage-gated ion channels. Females showed enrichments for cell polarity and differentiation, chemotaxis inhibition, gene silencing, and hormone and immune signaling. Notably, the majority of sex-biased genes in monomorphic RA were sex chromosome Z genes. These findings reveal a profound, sex-specific reorganization of RA’s transcriptome, providing novel insights into potential targets and drivers of sexually dimorphic neurodevelopment.

2022-07-14 | GSE191296 | GEO

Cocaine self-administration induces divergent protein expression in the nucleus accumbens of male and female mice to eliminate basal sex differences

Project description:Substance use disorder (SUD) is a chronic neuropsychiatric condition characterized by long-lasting alterations in the neural circuitry regulating reward and motivation. Substantial work has focused on characterizing the molecular substrates which underlie these persistent changes in neural function and behavior; however, this work has overwhelmingly focused on male subjects, despite mounting clinical and preclinical evidence that females demonstrate dissimilar progression to SUD and responsivity to drugs of abuse, such as cocaine. Here, we show that sex is a critical biological variable that defines drug-induced plasticity in the NAc. Using quantitative mass spectrometry, we assessed the protein expression patterns altered by cocaine self-administration and demonstrate unique molecular profiles between males and females. We show that 1. Cocaine self-administration induces non-overlapping protein expression patterns in males and females and 2. Cocaine specifically acts on baseline sexual dimorphisms to exert these effects. Critically, we find that cocaine administration blunts not only basal sex-differences in the accumbens proteome, but also the pre-existing sex differences in behavior for natural rewards. Together, these data suggest that chronic cocaine is capable of rewriting baseline proteomic function to maintain cocaine-specific behaviors.

2021-09-09 | PXD022832 | Pride

miRNA expression data from human myocardial infarction hearts

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome Human tissue samples, acquired during post-mortem examination and frozen in liquid nitrogen, were provided by the department of pathology, Tokyo Metropolitan Geriatric Hospital after the approval from the ethical committee. Age- and sex-matched cohorts were selected to compare healthy hearts to those with post-MI LV remodeling. Border zone for myocardial infarction was sampled. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress

Sex chromosome complement defines diffuse versus focal angiotensin II-induced aortic pathology

Project description:Objective-Aortic pathologies exhibit sexual dimorphism, with aneurysms in the ascending, thoracic and abdominal aorta (AAA) exhibiting higher prevalence in males. Despite lower incidence of aortic vascular disease in women, aneurysms progress rapidly. Mechanisms for these sex differences are unclear. We defined the role of sex chromosome complement and testosterone in regional development and progression of angiotensin II (AngII)-induced vascular pathologies. Approach and Results-We used transgenic male mice expressing Sry on an autosome to create low density lipoprotein receptor (Ldlr) deficient male mice with an XY or XX sex chromosome complement. Subjects were then sham operated or orcheictomized. Transcriptional profiling on abdominal aortas from XY or XX males demonstrated1746 genes influenced by sex chromosomes, sex hormones, or an interaction. A second cohort of animals was then infused with AngII for 28 days. Diffuse aortic aneurysm pathology developed in XY AngII-infused males, while XX males developed discrete AAAs. Castration reduced all AngII-induced aortic pathologies in XY and XX males. Thoracic aortas from AngII-infused XY males, but not XX males exhibited adventitial thickening. We infused male XY and XX mice with saline or AngII and quantified mRNA abundance of key genes in thoracic versus abdominal aortas. Regional differences in mRNA abundance existed before AngII infusions, which were differentially influenced by AngII between genotypes. Prolonged AngII infusions resulted in AAA aortic wall thickening in XY males with diffuse aortic pathology, while XX males had dilated focal AAAs. Conclusions-An XY sex chromosome complement mediates diffuse aortic pathology, while an XX sex chromosome complement contributes to discrete AngII-induced AAAs.

2018-07-22 | GSE102143 | GEO

miRNA expression data from human myocardial infarction hearts

2016-01-07 | GSE76591 | GEO

Differential regulation of mouse hippocampal gene expression sex differences by chromosomal content and gonadal sex: RNA-Seq Data

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