The developmental origins of sex-biased expression in cardiac development
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ABSTRACT:
PROVIDER: PRJNA557361 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9860440.fastq.gz | Fastqsanger.gz | |||
| SRR9860450.fastq.gz | Fastqsanger.gz | |||
| SRR9860441.fastq.gz | Fastqsanger.gz | |||
| SRR9860451.fastq.gz | Fastqsanger.gz | |||
| SRR9860442.fastq.gz | Fastqsanger.gz |
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Project description:Male and female disease states differ in their prevalence, treatment responses, and survival rates. In cardiac disease, women almost uniformly fare far worse than men1-3. Though sex plays a critical role in cardiac disease, the mechanisms underlying sex differences in cardiac homeostasis and disease remain unexplained. Here, we reveal sex-specific cardiac transcriptomes and proteomes and show that cardiac sex differences are predominately controlled via post-transcriptional mechanisms. Using a quantitative proteomics-based approach, we characterize differential sex-specific enriched cardiac proteins, protein complexes, and biological sex processes in the context of global genetic diversity of the Collaborative Cross. We show that differences in cardiac protein expression are established by both hormonal and genetic mechanisms and define two additional pathways, one that is SRY dependent and one that is SRY-independent. We also determined the onset of sex-biased protein expression and discovered that sex disparities in heart tissue occur at the earliest stages of heart development, during the period preceding primary mammalian sex determination. This may explain why congenital heart disease, a leading cause of death whose origin is often developmental, is sex biased. Our results reveal the molecular foundations for the differences in cardiac tissue that underlie sex disparities in health, disease, and treatment outcomes.
2022-08-11 | PXD020139 | Pride
Project description:We use a custom microarray for the crustacean Daphnia pulex to investigate gene expression in males, juvenile females and pregnant females. Keywords: sex-biased, developmental
2006-10-06 | GSE5908 | GEO
Project description:The sexually dimorphic gene expression profiles are established in early embryogenesis and epigenetically perpetuated at every stage of cardiac development.
2022-07-29 | GSE135084 | GEO
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:Genes with sex-biased expression in adults experience unique evolutionary dynamics. It is unclear, however, whether the selection pressures responsible for these well documented patterns also act upon genes with sex-biased expression in other developmental stages. To examine this, we measured expression in male and female Drosophila melanogaster larvae.
2012-04-08 | GSE31722 | GEO
Project description:BACKGROUND:Expression patterns between males and females vary in every adult tissue, even in organs with no conspicuous dimorphisms such as the heart. While studies of male and female differences have traditionally focused on the influence of sex hormones, these do not account for all the differences at the molecular and epigenetic levels. We previously reported that a substantial number of genes were differentially expressed in male and female mouse embryonic stem (ES) cells and revealed dose-dependent enhancer activity in response to Prdm14, a key pluripotency factor expressed more highly in female ES cells. In this work, we investigated the role of Prdm14 in establishing sex-specific gene expression networks. We surveyed the sex-specific landscape in early embryogenesis with special reference to cardiac development. We generated sex-specific co-expression networks from mouse ES cells, examined the presence of sex-specific chromatin domains, and analyzed previously published datasets from different developmental time points to characterize how sex-biased gene expression waxes and wanes to evaluate whether sex-biased networks are detectable throughout heart development. RESULTS:We performed ChIP-seq on male and female mouse ES cells to determine differences in chromatin status. Our study reveals sex-biased histone modifications, underscoring the potential for the sex chromosome complement to prime the genome differently in early development with consequences for later expression biases. Upon differentiation of ES cells to cardiac precursors, we found sex-biased expression of key transcription and epigenetic factors, some of which persisted from the undifferentiated state. Using network analyses, we also found that Prdm14 plays a prominent role in regulating a subset of dimorphic expression patterns. To determine whether sex-biased expression is present throughout cardiogenesis, we re-analyzed data from two published studies that sampled the transcriptomes of mouse hearts from 8.5 days post-coitum embryos to neonates and adults. We found sex-biased expression at every stage in heart development, and interestingly, identified a subset of genes that exhibit the same bias across multiple cardiogenic stages. CONCLUSIONS:Overall, our results support the existence of sexually dimorphic gene expression profiles and regulatory networks at every stage of cardiac development, some of which may be established in early embryogenesis and epigenetically perpetuated.
| S-EPMC6727560 | biostudies-literature
Project description:The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages.
2016-04-06 | GSE77794 | GEO
Project description:The difference in X chromosome copy number creates a potential difference in X chromosomal gene expression between males and females. In many animals, dosage compensation mechanisms equalize X chromosome expression between sexes. Yet, X chromosome is also enriched for sex-biased genes due to differences in the evolutionary history of the X and autosomes. The manner in which dosage compensation and sex-biased gene expression exist on the X chromosome remains an open question. Most studies compare gene expression between two sexes, which combines expression differences due to X chromosome number (dose) and sex. Here, we uncoupled the effects of sex and X dose in C. elegans and determined how each process affects expression of the X chromosome compared to autosomes. We found that in the soma, sex-biased expression on the X chromosome is almost entirely due to sex because the dosage compensation complex (DCC) effectively compensates for the X dose difference between sexes. In the germline where the DCC is not present, X chromosome copy number contributes to hermaphrodite-biased gene expression. These results suggest that X dose contributes to sex-biased gene expression based on the level of dosage compensation in different tissues and developmental stages. RNA-Seq profiles of C. elegans XO hermaphrodite and XX male L3 larvae and adults
2016-04-06 | E-GEOD-77794 | 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: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