Ontology highlight
ABSTRACT:
PROVIDER: PRJNA553192 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9652630_1.fastq.gz | Fastqsanger.gz | |||
| SRR9652630_2.fastq.gz | Fastqsanger.gz | |||
| SRR9652640.fastq.gz | Fastqsanger.gz | |||
| SRR9652640_1.fastq.gz | Fastqsanger.gz | |||
| SRR9652640_2.fastq.gz | Fastqsanger.gz |
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Project description:Sex determination evolves rapidly, often because of turnover of the genes at the top of the pathway. The house fly, Musca domestica, has a multifactorial sex determination system, allowing us to identify the selective forces responsible for the evolutionary turnover of sex determination in action. There is a male determining factor, M, on the Y chromosome (Y^M), which is probably the ancestral state. An M factor on the third chromosome (III^M) has reached high frequencies in multiple populations across the world, but the evolutionary forces responsible for the invasion of III^M are not resolved. To test if the III^M chromosome invaded because of sex-specific selection pressures, we used mRNA sequencing to determine if isogenic males that differ only in the presence of the Y^M or III^M chromosome have different gene expression profiles. We find that more genes are differentially expressed between Y^M and III^M males in testis than head, and that genes with male-biased expression are most likely to be differentially expressed between Y^M and III^M males. This suggests that male phenotypes, especially those related to male fertility, are more likely to be affected by the male-determining chromosome, supporting the hypothesis that sex-specific selection acts on alleles linked to the male-determining locus driving evolutionary turnover in the sex determination pathway. We additionally find that III^M males have a "masculinization" gene expression profile, suggesting that the III^M chromosome has accumulated an excess of male-beneficial alleles because of its male-limited transmission.
2015-03-20 | GSE67065 | GEO
Project description:Recent studies have revealed key roles of non-coding RNAs in sex-related pathways, but little is known about the evolutionary forces acting on these non-coding RNAs. We used whole-genome tiling arrays to profile the transcriptome of Drosophila melanogaster tissues and found that 15% of male-biased transcribed fragments (transfrags) are intergenic non-coding RNAs (incRNAs), suggesting a potentially important role for incRNAs in sex-related biological processes. Statistical analysis revealed a paucity of male-biased incRNAs and coding genes on the X chromosome, suggesting that similar evolutionary forces could be affecting the genomic organization of both coding and non-coding genes. Expression profiling across germline and somatic tissues further suggests that both male meiotic sex chromosome inactivation (MSCI) and sexual antagonism contribute to the chromosomal distribution of male-biased incRNAs. Comparative sequence analysis shows that the evolutionary age of male-biased incRNAs is a significant predictor of their chromosomal locations. In addition to identifying abundant sex-biased incRNAs in fly genome, our work unveils a global picture of the complex interplay between non-coding RNAs and sexual chromosome evolution.
2013-12-18 | GSE53421 | GEO
Project description:Decades ago, evidence of age-related reactivation of a single gene on the female inactive X chromosome was observed in mice. While stable silencing of the Barr body is crucial for balancing gene dosage between sexes, it remained unclear whether silencing is maintained during aging. Here, we employed allele-specific multi-omics approaches to capture a comprehensive catalog of genes escaping X chromosome inactivation throughout mouse development and aging. We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions. Consistently, chromatin accessibility was increased across multiple megabases at chromosome ends, affecting regulatory elements of escapees. Since several age-specific escapees are linked to human diseases, their elevated expression in females might contribute to sex-biased disease progression observed during aging.
2025-03-21 | GSE274694 | GEO
Project description:Recent studies have revealed key roles of non-coding RNAs in sex-related pathways, but little is known about the evolutionary forces acting on these non-coding RNAs. We used whole-genome tiling arrays to profile the transcriptome of Drosophila melanogaster tissues and found that 15% of male-biased transcribed fragments (transfrags) are intergenic non-coding RNAs (incRNAs), suggesting a potentially important role for incRNAs in sex-related biological processes. Statistical analysis revealed a paucity of male-biased incRNAs and coding genes on the X chromosome, suggesting that similar evolutionary forces could be affecting the genomic organization of both coding and non-coding genes. Expression profiling across germline and somatic tissues further suggests that both male meiotic sex chromosome inactivation (MSCI) and sexual antagonism contribute to the chromosomal distribution of male-biased incRNAs. Comparative sequence analysis shows that the evolutionary age of male-biased incRNAs is a significant predictor of their chromosomal locations. In addition to identifying abundant sex-biased incRNAs in fly genome, our work unveils a global picture of the complex interplay between non-coding RNAs and sexual chromosome evolution. We used whole-genome tiling arrays to assess sex-biased transcription in D. melanogaster adult whole bodies, and testis, ovary, and accessory gland samples. Gut and thorax, tissues expected to exhibit little or no sex-biased expression, were included as controls. Expression was measured in 2-4 replicates for each tissue.
2013-12-18 | E-GEOD-53421 | biostudies-arrayexpress
Project description:Decades ago, evidence of age-related reactivation of a single gene on the female inactive X chromosome was observed in mice. While stable silencing of the Barr body is crucial for balancing gene dosage between sexes, it remained unclear whether silencing is maintained during aging. Here, we employed allele-specific multi-omics approaches to capture a comprehensive catalog of genes escaping X chromosome inactivation throughout mouse development and aging. We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions. Consistently, chromatin accessibility was increased across multiple megabases at chromosome ends, affecting regulatory elements of escapees. Since several age-specific escapees are linked to human diseases, their elevated expression in females might contribute to sex-biased disease progression observed during aging.
2025-03-21 | GSE274692 | GEO
Project description:Decades ago, evidence of age-related reactivation of a single gene on the female inactive X chromosome was observed in mice. While stable silencing of the Barr body is crucial for balancing gene dosage between sexes, it remained unclear whether silencing is maintained during aging. Here, we employed allele-specific multi-omics approaches to capture a comprehensive catalog of genes escaping X chromosome inactivation throughout mouse development and aging. We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions. Consistently, chromatin accessibility was increased across multiple megabases at chromosome ends, affecting regulatory elements of escapees. Since several age-specific escapees are linked to human diseases, their elevated expression in females might contribute to sex-biased disease progression observed during aging.
2025-03-21 | GSE274690 | GEO
Project description:Decades ago, evidence of age-related reactivation of a single gene on the female inactive X chromosome was observed in mice. While stable silencing of the Barr body is crucial for balancing gene dosage between sexes, it remained unclear whether silencing is maintained during aging. Here, we employed allele-specific multi-omics approaches to capture a comprehensive catalog of genes escaping X chromosome inactivation throughout mouse development and aging. We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions. Consistently, chromatin accessibility was increased across multiple megabases at chromosome ends, affecting regulatory elements of escapees. Since several age-specific escapees are linked to human diseases, their elevated expression in females might contribute to sex-biased disease progression observed during aging.
2025-03-21 | GSE274689 | GEO
Project description:Birds have a sex chromosome system in which females are heterogametic (ZW) and males are homogametic (ZZ). The differentiation of avian sex chromosomes from ancestral autosomes entailed the loss of most genes from the W chromosome during evolution. However, to what extent mechanisms evolved that counterbalance the consequences of this extensive gene dosage reduction in female birds has remained unclear. Here we report functional in vivo and evolutionary analyses of a Z-chromosome-linked microRNA (miR-2954) with strongly male-biased expression that was previously proposed to play a key role in sex chromosome dosage compensation1. We knocked out miR-2954 in chicken, which resulted in early embryonic lethality of homozygous knockout males, likely due to the highly specific upregulation of dosage-sensitive Z-linked target genes of miR-2954. Our evolutionary gene expression analyses further revealed that these dosage-sensitive target genes have become upregulated on the single Z in female birds during evolution. Altogether, our work unveils a scenario where evolutionary pressures on females following W gene loss led to the evolution of transcriptional upregulation of dosage-sensitive genes on the Z not only in female but also in male birds. The resulting overabundance of transcripts in males resulting from the combined activity of two dosage-sensitive Z gene copies was in turn offset by the emergence of a highly targeted miR-2954-mediated transcript degradation mechanism during avian evolution. Our findings demonstrate that birds have evolved a unique sex chromosome dosage compensation system in which a microRNA has become essential for male survival.
2024-04-17 | GSE257549 | GEO
Project description:Skewed X-chromosome inactivation (XCI) plays an important role in the phenotypic heterogeneity of X-linked disorders. However, the role of skewed XCI in XCI–escaping gene SHOX regulation is unclear. Here, we focused on a heterozygous deletion of SHOX gene enhancer with clinical heterogeneity. Using SNP array, we detected that the female proband with Leri-Weill dyschondrosteosis (LWD) carried an 857 kb deletion on Xp22.3 (encompassing SHOX enhancer) and a 5,707 kb large-fragment deletion on Xq25q26. XCI analysis revealed that the X-chromosome with the Xq25q26 large-fragment deletion was completely inactivated, which forced the complete activation of the other X-chromosome carrying SHOX enhancer deletion. While the Xp22.3 deletion locates on the escaping XCI region, under the combined action of skewed XCI and escaping XCI, transcription of SHOX gene was mainly from the activated X-chromosome with SHOX enhancer defect, involving in the formation of LWD phenotype. Interestingly, this SHOX enhancer deletion was inherited from her healthy mother, who also demonstrated completely skewed XCI. However, the X-chromosome with SHOX enhancer deletion was inactivated, and the normal X-chromosome was activated. Combing with escaping XCI, her phenotype was almost normal. In summary, this study was a rare report of SHOX gene enhancer deletion in a family with clinical heterogeneity due to skewed inactivation of different X-chromosomes, which can help in the genetic counseling and prenatal diagnosis of disorders in females with SHOX defect.
2019-10-08 | GSE138489 | GEO