The effect of Bcl6 on liver sex difference
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ABSTRACT:
PROVIDER: PRJNA420073 | ENA |
REPOSITORIES: ENA
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Project description:To confirm the effect of Bcl6 on the liver sex difference, we performed the gene expression analysis in male and female wild type mice and male and female liver specific Bcl-6 deficient mice.
2017-11-29 | GSE107435 | GEO
Project description:To confirm the effect of Bcl6 on the liver sex differrence, we performed the gene expression analysis in male and female wile type mice and male and female liver specific Bcl-6 deficient mice.
2017-01-19 | GSE89091 | GEO
Project description:The effect of Bcl6-downstream transcription factors on the liver sex difference
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Project description:To confirm the effect of Bcl6-downstream transcription factors, Cux2, Sall1, Trim24, on the liver sex differrence, we performed the gene expression analysis in male and female Cas9-knockin mice.
2025-11-25 | GSE310488 | GEO
Project description:Sex-dependent pituitary growth hormone (GH) secretory patterns determine the sex-biased expression of >1,000 genes in mouse and rat liver, affecting lipid and drug metabolism, inflammation and disease. A fundamental biological question is how robust differential expression can be achieved for hundreds of sex-biased genes simply based on the GH input signal pattern: pulsatile GH stimulation in males vs. near-continuous GH exposure in females. STAT5 is an essential transcriptional mediator of the sex-dependent effects of GH in the liver, but the mechanisms that underlie its sex-dependent actions are obscure. Here we elucidate the dynamic, sex-dependent binding of STAT5 and the GH/STAT5-regulated repressor BCL6 to mouse liver chromatin, revealing the counteractive interplay between these two regulators of liver sex-specificity. Our findings establish a close correlation between sex-dependent STAT5 binding and sex-biased target gene expression. Moreover, sex-dependent STAT5 binding correlated positively with sex-biased DNase hypersensitivity and H3-K4me1 and H3-K4me3 (activating) marks, correlated negatively with sex-biased H3-K27me3 (repressive) marks, and was associated with sex-differentially enriched motifs for HNF6/CDP factors. Importantly, BCL6 binding was preferentially associated with repression of female-biased STAT5 targets in male liver. Furthermore, BCL6 and STAT5 common targets but not BCL6 unique targets showed strong enrichment for lipid and drug metabolism. These findings provide a comprehensive, genome-wide view of the mechanisms whereby these two GH-regulated transcription factors establish and maintain sex differences affecting liver physiology and disease. The approaches used here to characterize sex-dependent STAT5 and BCL6 binding can be applied to other condition-specific regulatory factors and binding sites and their interplay with co-operative chromatin-binding factors.
2011-12-18 | GSE31578 | GEO
Project description:Sex-dependent pituitary growth hormone (GH) secretory patterns determine the sex-biased expression of >1,000 genes in mouse and rat liver, affecting lipid and drug metabolism, inflammation and disease. A fundamental biological question is how robust differential expression can be achieved for hundreds of sex-biased genes simply based on the GH input signal pattern: pulsatile GH stimulation in males vs. near-continuous GH exposure in females. STAT5 is an essential transcriptional mediator of the sex-dependent effects of GH in the liver, but the mechanisms that underlie its sex-dependent actions are obscure. Here we elucidate the dynamic, sex-dependent binding of STAT5 and the GH/STAT5-regulated repressor BCL6 to mouse liver chromatin, revealing the counteractive interplay between these two regulators of liver sex-specificity. Our findings establish a close correlation between sex-dependent STAT5 binding and sex-biased target gene expression. Moreover, sex-dependent STAT5 binding correlated positively with sex-biased DNase hypersensitivity and H3-K4me1 and H3-K4me3 (activating) marks, correlated negatively with sex-biased H3-K27me3 (repressive) marks, and was associated with sex-differentially enriched motifs for HNF6/CDP factors. Importantly, BCL6 binding was preferentially associated with repression of female-biased STAT5 targets in male liver. Furthermore, BCL6 and STAT5 common targets but not BCL6 unique targets showed strong enrichment for lipid and drug metabolism. These findings provide a comprehensive, genome-wide view of the mechanisms whereby these two GH-regulated transcription factors establish and maintain sex differences affecting liver physiology and disease. The approaches used here to characterize sex-dependent STAT5 and BCL6 binding can be applied to other condition-specific regulatory factors and binding sites and their interplay with co-operative chromatin-binding factors. Mouse livers were excised from individual male and female mice killed at either a peak of STAT5 binding activity, or during the growth hormone (GH) interpulse interval, when STAT5 activity is either low (females) or essentially undetectable (males). Sonicated, cross-linked liver nuclear chromatin was then used to identify STAT5 binding sites by ChIP-Seq.
2011-12-18 | E-GEOD-31578 | biostudies-arrayexpress
Project description:Animal models are important tools in scientific research, whereas the animals used are usually single-sex instead of mixed-sex in the experimental design. To better understand the effect of sex difference, we compared several phenotypes between male and female C57BL/6 mice, including behavioral tests, plasma corticosterone levels, adult neurogenesis, and RNA-seq. The experiments were performed under non-stressed and chronic-stressed conditions, respectively. Overall, our results showed several differences between male and female mice in sensorimotor performance while little difference was found in anxiety, depression, learning, and memory. We did not observe a significant difference in adult neurogenesis. There was a sex difference in plasma corticosterone levels under chronic stress conditions, either in 30 min after the restraint stress or after 60min of the recovery. Yet, the corticosterone levels were equivalent between the sexes under non-stressed conditions at any time point. Furthermore, the results of RNA-seq identified the differential expression genes between male and female mice under non-stressed or chronic-stressed conditions.
2022-08-22 | GSE211276 | GEO
Project description:Bile acid (BA) metabolism must be tightly regulated because BAs serve as metabolic signaling molecules but become cytotoxic at high levels. The farnesoid X receptor (FXR) is a crucial bile acid sensor, but our understanding of its regulation and coordination with other transcription factors is limited. Here, we found that B cell lymphoma 6 (Bcl6) functions along with FXR to control bile acid levels. We found that mice lacking hepatic BCL6 (Bcl6LKO) had increased BA synthesis and serum levels. In line with this, Bcl6LKO mice had elevated serum cholesterol, the upstream substrate for BA synthesis, as well as reduced expression of the hepatic BA re-uptake transporter sodium-taurocholate cotransporting polypeptide (NTCP). Furthermore, loss of BCL6 reduced hepatic fibroblast growth factor 4 (FGFR4) expression, causing dysregulated entero-hepatic BA feedback signaling. To better understand the relative contribution of BCL6 and FXR in regulating BA homeostasis, we generated mice with a combined deletion of hepatic BCL6 and FXR (Bcl6LKOFxrKO). Critically, combined deletion of FXR and hepatic BCL6 caused massive elevations in BA synthesis/levels compared to loss of Fxr or Bcl6 alone, which resulted in cholestatic liver damage. Mechanistically, we found that Bcl6LKO FxrKO mice had an almost complete loss of hepatic Shp expression, causing high levels of the rate-limiting BA synthesis enzyme CYP7A1. Together, these findings demonstrate that BCL6 and FXR function together to limit BA synthesis and protect the liver from cholestatic injury.
2026-02-11 | GSE296552 | GEO
Project description:Sex-biased and random monoallelic expression of SHOX: implications for sex difference in height
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