Bioreactor sludge metagenome
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ABSTRACT:
PROVIDER: PRJDB11428 | ENA |
REPOSITORIES: ENA
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Project description:Haplotype-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this phenomenon using stringent criteria in disease-relevant tissues remain sparse. Here we apply array-based and Methyl-seq approaches to multiple human tissues and cell types, including brain, purified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM differentially methylated regions (DMRs) and 3,082 strong methylation quantitative trait loci (mQTLs), most not previously reported. More than half of these DMRs have cell type-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs located near GWAS signals for immune and neurological disorders. Targeted bis-seq confirmed hap-ASM in 12/13 loci tested, including CCDC155, CD69, FRMD1, IRF1, KBTBD11, and S100A*-ILF2, associated with immune phenotypes, MYT1L, PTPRN2,CMTM8 and CELF2, associated with neurological disorders, NGFR and HLA-DRB6, associated with both immunological and brain disorders, and ZFP57, a trans-acting regulator of genomic imprinting. Polymorphic CTCF and transcription factor (TF) binding sites are over-represented among hap-ASM DMRs and mQTLs, and analysis of the human data, supplemented by cross-species comparisons to Macaca mulattamacaques, indicates that CTCF and TF binding likelihood predicts the strength and direction of the allelic methylation asymmetry. These results show that hap-ASM is highly tissue-specific; an important trans-acting regulator of genomic imprinting is regulated by this phenomenon; variation in CTCF and TF binding sites is an underlying mechanism in primary tissues, and maps of hap-ASM and mQTLs reveal regulatory sequences underlying supera- and sub-threshold GWAS peaks in immunological and neurological disorders.
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Project description:Haplotype-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this phenomenon using stringent criteria in disease-relevant tissues remain sparse. Here we apply array-based and Methyl-seq approaches to multiple human tissues and cell types, including brain, purified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM differentially methylated regions (DMRs) and 3,082 strong methylation quantitative trait loci (mQTLs), most not previously reported. More than half of these DMRs have cell type-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs located near GWAS signals for immune and neurological disorders. Targeted bis-seq confirmed hap-ASM in 12/13 loci tested, including CCDC155, CD69, FRMD1, IRF1, KBTBD11, and S100A*-ILF2, associated with immune phenotypes, MYT1L, PTPRN2,CMTM8 and CELF2, associated with neurological disorders, NGFR and HLA-DRB6, associated with both immunological and brain disorders, and ZFP57, a trans-acting regulator of genomic imprinting. Polymorphic CTCF and transcription factor (TF) binding sites are over-represented among hap-ASM DMRs and mQTLs, and analysis of the human data, supplemented by cross-species comparisons to Macaca mulattamacaques, indicates that CTCF and TF binding likelihood predicts the strength and direction of the allelic methylation asymmetry. These results show that hap-ASM is highly tissue-specific; an important trans-acting regulator of genomic imprinting is regulated by this phenomenon; variation in CTCF and TF binding sites is an underlying mechanism in primary tissues, and maps of hap-ASM and mQTLs reveal regulatory sequences underlying supera- and sub-threshold GWAS peaks in immunological and neurological disorders.
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Project description:Haplotype-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this phenomenon using stringent criteria in disease-relevant tissues remain sparse. Here we apply array-based and Methyl-seq approaches to multiple human tissues and cell types, including brain, purified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM differentially methylated regions (DMRs) and 3,082 strong methylation quantitative trait loci (mQTLs), most not previously reported. More than half of these DMRs have cell type-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs located near GWAS signals for immune and neurological disorders. Targeted bis-seq confirmed hap-ASM in 12/13 loci tested, including CCDC155, CD69, FRMD1, IRF1, KBTBD11, and S100A*-ILF2, associated with immune phenotypes, MYT1L, PTPRN2,CMTM8 and CELF2, associated with neurological disorders, NGFR and HLA-DRB6, associated with both immunological and brain disorders, and ZFP57, a trans-acting regulator of genomic imprinting. Polymorphic CTCF and transcription factor (TF) binding sites are over-represented among hap-ASM DMRs and mQTLs, and analysis of the human data, supplemented by cross-species comparisons to Macaca mulattamacaques, indicates that CTCF and TF binding likelihood predicts the strength and direction of the allelic methylation asymmetry. These results show that hap-ASM is highly tissue-specific; an important trans-acting regulator of genomic imprinting is regulated by this phenomenon; variation in CTCF and TF binding sites is an underlying mechanism in primary tissues, and maps of hap-ASM and mQTLs reveal regulatory sequences underlying supera- and sub-threshold GWAS peaks in immunological and neurological disorders.
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Project description:Over-expression of human angiotensin-II receptor type1 (hAT1R) may cause pathological outcomes due to overactivation of renin-angiotensin system. Transgenic (TG) mice containing Hap-I (hypertensive genotype) of human hAT1R gene are more prone to develop metabolic syndrome disorders as compared to TG mice with Hap-II (normotensive genotype). This gene variant associated risk of hypertension together with Western diet and aging may lead to renal disorders. However, mechanisms underlying this process are not well examined. For this purpose, we studied the renal gene expression alterations in aged TG mice containing either Hap-I or Hap-II of hAT1R gene. Aged mice (20-24 months of age) were maintained on a regular diet or high fat diet with 2% NaCl (Western diet, WD) for 16 weeks. On a regular diet, aged Hap-I mice presented higher (~9 mmHg) systolic blood pressure with respect to age-matched Hap-II animals. Following administration of Western diet, blood pressure increased in both groups of mice, but to a larger extent in Hap-I animals (~15 mmHg in comparison to ~7 mmHg in Hap-II). Aged Hap-I mice on Western diet showed increased renal fibrosis. RNA-seq data from renal tissue of Hap-I aged mice revealed that WD significantly altered the expression of >400 genes (p-adj. <0.05). Bioinformatics analysis (Qiagen IPA software) identified major alterations in main canonical pathways involved in renal function and oxidative damage. These changes in turn resulted in kidney failure, renal tubular injury, and renal proliferation. In addition, post WD treatment, RNA seq. analysis from Hap-I and Hap-II kidneys also reveals haplotype specific regulation of genes associated with blood pressure regulation and kidney disorders. Overall, these results indicate that Western diet promotes hypertension and fibrosis in the kidneys of aged mice. These alterations are paralleled by perturbation of renal transcriptional profile. Overall, these studies will assist in the identification of novel mechanisms and molecules involved in hypertension and associated kidney pathophysiology.
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Project description:Over-expression of human angiotensin-II receptor type1 (hAT1R) may cause pathological outcomes due to overactivation of renin-angiotensin system. Transgenic (TG) mice containing Hap-I (hypertensive genotype) of human hAT1R gene are more prone to develop metabolic syndrome disorders as compared to TG mice with Hap-II (normotensive genotype). This gene variant associated risk of hypertension together with Western diet and aging may lead to renal disorders. However, mechanisms underlying this process are not well examined. For this purpose, we studied the renal gene expression alterations in aged TG mice containing either Hap-I or Hap-II of hAT1R gene. Aged mice (20-24 months of age) were maintained on a regular diet or high fat diet with 2% NaCl (Western diet, WD) for 16 weeks. On a regular diet, aged Hap-I mice presented higher (~9 mmHg) systolic blood pressure with respect to age-matched Hap-II animals. Following administration of Western diet, blood pressure increased in both groups of mice, but to a larger extent in Hap-I animals (~15 mmHg in comparison to ~7 mmHg in Hap-II). Aged Hap-I mice on Western diet showed increased renal fibrosis. RNA-seq data from renal tissue of Hap-I aged mice revealed that WD significantly altered the expression of >400 genes (p-adj. <0.05). Bioinformatics analysis (Qiagen IPA software) identified major alterations in main canonical pathways involved in renal function and oxidative damage. These changes in turn resulted in kidney failure, renal tubular injury, and renal proliferation. In addition, post WD treatment, RNA seq. analysis from Hap-I and Hap-II kidneys also reveals haplotype specific regulation of genes associated with blood pressure regulation and kidney disorders. Overall, these results indicate that Western diet promotes hypertension and fibrosis in the kidneys of aged mice. These alterations are paralleled by perturbation of renal transcriptional profile. Overall, these studies will assist in the identification of novel mechanisms and molecules involved in hypertension and associated kidney pathophysiology.
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