Ontology highlight
ABSTRACT:
PROVIDER: PRJNA951902 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24058500_1.fastq.gz | Fastqsanger.gz | |||
| SRR24058500_2.fastq.gz | Fastqsanger.gz | |||
| SRR24058501_1.fastq.gz | Fastqsanger.gz | |||
| SRR24058501_2.fastq.gz | Fastqsanger.gz | |||
| SRR24058502_1.fastq.gz | Fastqsanger.gz |
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Project description:Sequencing files provided here include 4C-seq experiments for a total of 6 viewpoints neighboring 5 highly sex-biased genes in mouse liver. These files are part of a larger study ("CTCF and Cohesin link sex-biased distal regulatory elements to sex-biased gene expression in mouse liver"), where we compare CTCF and cohesin binding in male and female mouse liver as well as differences in chromatin conformation (DNA looping).
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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). Examination of six different histone modifications in male and female mouse liver.
2013-07-03 | E-GEOD-44571 | biostudies-arrayexpress
Project description:Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21. These files are part of a larger study ("CTCF and Cohesin link sex-biased distal regulatory elements to sex-biased gene expression in mouse liver") where we compare CTCF and cohesin binding in male and female mouse liver as well as differences in chromatin conformation (DNA looping).
2020-07-07 | GSE130908 | 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:Heterozygous point mutations or genomic deletions of NR0B1 in Xp21.2 result in congenital adrenal hypoplasia and hypogonadotropic hypogonadism, whereas the NR0B1 locus duplications in XY individuals lead to gonadal dysgenesis and a male-to-female dosage-sensitive sex reversal. We previously reported an ~ 257 kb deletion mapping 11 kb upstream to NR0B1 in a XY female with primary amenorrhea, small immature uterus, and gonadal dysgenesis pointing to an alteration of its regulatory region. To identify the potential regulatory elements of NR0B1, we have analyzed its 2 Mb flanking regions using chromosome conformation capture-on-chip (4C) in Sertoli cells and lymphoblasts. We confirm the involvement of the previously proposed regulatory region in the control of NR0B1 expression and describe several novel potential chromatin interactions within the NR0B1 locus that may be involved in sex differentiation. Custom designed 3x720K tiling microarrays covering 4 Mb region (chrX:28,082,100-32,087,100) flanking NR0B1 gene of interest
2014-12-24 | E-GEOD-64470 | biostudies-arrayexpress
Project description:∼40,000 HNF6 binding sites were identified in mouse liver chromatin, including several thousand sites showing significant differences in level of HNF6 binding between male and female mouse liver. These sex-biased HNF6 binding sites showed strong enrichment for sex-biased DNase hypersensitive sites and for proximity to genes showing local sex-biased chromatin marks and a corresponding sex-biased expression. ~90% of genome-wide CUX2 binding sites identified previously in female mouse liver (Conforto TL, Zhang Y, Sherman J, Waxman DJ., Mol Cell Biol. 2012;32(22):4611-4627) were also bound by HNF6, giving evidence for genome-wide competition between HNF6 and CUX2 for chromatin binding in female mouse liver. These HNF6/CUX2 common binding sites were enriched for genomic regions more accessible in male than in female mouse liver chromatin, and showed strongest enrichment for male-biased genes, suggesting HNF6 displacement by CUX2 as a mechanism to explain the observed CUX2 repression of male-biased genes in female liver. However, HNF6 binding was sex-independent at a majority of its binding sites, and peak regions of HNF6 binding were frequently associated with co-binding by multiple other liver transcription factors, consistent with HNF6 playing a global regulatory role in both male and female liver. Livers were excised from individual male and female mice, cross-linked and sonicated, then used to identify HNF6 binding sites by ChIP-Seq using antibody specific to HNF6 (sc-13050; Santa Cruz Biotechnology, Inc).
2015-07-28 | E-GEOD-60014 | biostudies-arrayexpress
Project description:Heterozygous point mutations or genomic deletions of NR0B1 in Xp21.2 result in congenital adrenal hypoplasia and hypogonadotropic hypogonadism, whereas the NR0B1 locus duplications in XY individuals lead to gonadal dysgenesis and a male-to-female dosage-sensitive sex reversal. We previously reported an ~ 257 kb deletion mapping 11 kb upstream to NR0B1 in a XY female with primary amenorrhea, small immature uterus, and gonadal dysgenesis pointing to an alteration of its regulatory region. To identify the potential regulatory elements of NR0B1, we have analyzed its 2 Mb flanking regions using chromosome conformation capture-on-chip (4C) in Sertoli cells and lymphoblasts. We confirm the involvement of the previously proposed regulatory region in the control of NR0B1 expression and describe several novel potential chromatin interactions within the NR0B1 locus that may be involved in sex differentiation.
2014-12-24 | GSE64470 | GEO
Project description:∼40,000 HNF6 binding sites were identified in mouse liver chromatin, including several thousand sites showing significant differences in level of HNF6 binding between male and female mouse liver. These sex-biased HNF6 binding sites showed strong enrichment for sex-biased DNase hypersensitive sites and for proximity to genes showing local sex-biased chromatin marks and a corresponding sex-biased expression. ~90% of genome-wide CUX2 binding sites identified previously in female mouse liver (Conforto TL, Zhang Y, Sherman J, Waxman DJ., Mol Cell Biol. 2012;32(22):4611-4627) were also bound by HNF6, giving evidence for genome-wide competition between HNF6 and CUX2 for chromatin binding in female mouse liver. These HNF6/CUX2 common binding sites were enriched for genomic regions more accessible in male than in female mouse liver chromatin, and showed strongest enrichment for male-biased genes, suggesting HNF6 displacement by CUX2 as a mechanism to explain the observed CUX2 repression of male-biased genes in female liver. However, HNF6 binding was sex-independent at a majority of its binding sites, and peak regions of HNF6 binding were frequently associated with co-binding by multiple other liver transcription factors, consistent with HNF6 playing a global regulatory role in both male and female liver.
2015-07-28 | GSE60014 | GEO
Project description:Background Adolescent idiopathic scoliosis (AIS) is a complex spinal deformity characterized by three-dimensional curvature of the spine with an unknown etiology. Previous genome-wide association studies have identified a single-nucleotide polymorphism (rs6137473) located downstream of PAX1, which is significantly associated with female AIS risk. Methods To investigate the role of this region in spinal development and AIS pathogenesis, we generated a mouse model with deletion of a nearby conserved sex-associated region (Pax1-SARΔ). Spines were examined by both micro-CT and histology. Gene expression analysis (by RNA-sequencing and quantitative PCR) was carried out on E12.5 and E18.5 developing spines. Glycosaminoglycan (GAG) content was also measured by high-performance liquid chromatography. Results Micro-CT analysis revealed increased vertebral rotation at T4 in female Pax1-SARΔ mice at 4 months and at T9 in male Pax1-SARΔ mice at 6 months, along with kyphotic and lordotic sagittal curvatures. Histological examination revealed significant intervertebral disc degeneration, with the most severe changes observed in the female Pax1-SARΔ mice. GAG analysis found decreased chondroitin sulfate and dermatan sulfate content in male and female Pax1-SARΔ mice. Gene expression analysis at E12.5 showed upregulation of Pax1, Stat3, Ar, Foxa2, and Nkx2.2, while RNA-sequencing at E18.5 revealed sex-dependent changes in gene expression related to extracellular matrix components, immune and inflammatory responses, and scoliosis. Conclusion: These findings highlight the pivotal role of the Pax1 sex-associated genomic region in the development and maintenance of functional cartilage, extracellular matrix integrity, and intervertebral disc health, offering insights into the mechanisms underlying spinal degeneration and instability in AIS.
2026-05-14 | GSE324970 | GEO
Project description:Idiopathic scoliosis (IS) is a three-dimensional rotation of the spine >10 degrees with an unknown etiology. Our laboratory established a late-onset IS model in zebrafish (Danio rerio) containing a deletion in kif7. 25% of kif7co63/co63 zebrafish develop spinal curvatures and are otherwise developmentally normal, although the molecular mechanisms underlying the scoliosis are unknown. To define transcripts associated with scoliosis in this model, we performed bulk mRNA sequencing on 6 weeks past fertilization (wpf) kif7co63/co63 zebrafish with and without scoliosis. Additionally, we sequenced kif7co63/co63, kif7co63/+, and AB zebrafish (n= 3 per genotype). Sequencing reads were aligned to the GRCz11 genome and FPKM values were calculated. Differences between groups were calculated for each transcript by t-test. Principal component analysis showed that transcriptomes clustered by sample age and genotype. kif7 mRNA was mildly reduced in both homozygous and heterozygous zebrafish compared to AB. Sonic hedgehog target genes were upregulated in kif7co63/co63 zebrafish over AB, but no difference was detected between scoliotic and non-scoliotic mutants. The top upregulated genes in scoliotic zebrafish were cytoskeletal keratins.. Pankeratin staining of 6 wpf scoliotic and non-scoliotic kif7co63/co63 zebrafish showed increased keratin levels within the zebrafish musculature and intervertebral disc (IVD). Keratins are major components of the embryonic notochord, and aberrant keratin expression has been associated with intervertebral disc degeneration (IVDD) in both zebrafish and humans. The role of increased keratin accumulation as a molecular mechanism associated with the onset of scoliosis warrants further study.
2023-05-03 | GSE231606 | GEO