Ontology highlight
ABSTRACT:
PROVIDER: PRJNA698641 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq,and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice fed with control diet or low-protein diet.
2020-03-09 | GSE123254 | GEO
Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq,and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice fed with control diet or low-protein diet.
2020-03-09 | GSE123252 | GEO
Project description:The global prevalence of type 2 diabetes (T2D) is increasing, and it is contributing to the susceptibility to diabetes and its related epidemic in offspring. Although the impacts of paternal T2D on metabolism of offspring have been well established, the exact molecular and mechanistic basis that mediates these impacts remains largely unclear. Here we show that paternal T2D increases the susceptibility to diabetes in offspring through the gametic epigenetic alterations. Paternal T2D led to glucose intolerance and insulin resistance in offspring. Relative to controls, offspring of T2D fathers exhibited altered gene expression patterns in the pancreatic islets, with downregulation of several genes involved in glucose metabolism and insulin signaling pathway. Epigenomic profiling of offspring pancreatic islets revealed numerous changes in cytosine methylation depending on paternal T2D, including reproducible changes in methylation over several insulin signaling genes. Paternal T2D altered overall methylome patterns in sperm, with a large portion of differentially methylated genes overlapped with that of pancreatic islets in offspring. Our study revealed, for the first time, that T2D can be inherited transgenerationally through the mammalian germline by an epigenetic manner. Examination of the effect of paternal T2D on the DNA methylation in the pancreatic islets of offspring and in the sperm of father.
2013-01-02 | E-GEOD-43238 | biostudies-arrayexpress
Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq,and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice.
2020-03-17 | GSE123343 | GEO
Project description:Purpose: Paternal life experiences impact offspring health via germline, and epigenetic inheritance provides a potential mechanism. However, global reprogramming during offspring embryogenesis and gametogenesis represents the largest hurdle to conceptualize it. Yet, detailed characterization of how sperm epigenetic alterations carrying “environmental memory” can evade offspring embryonic reprogramming remains elusive. Methods: we profiled the sperm DNA methylation patterns of three consecutive generations (F0, F1 and F2) in both control and stress groups by using whole-genome bisulfite sequencing (WGBS). A total of 18 sperm samples were analyzed, including three biological replicates for each generation under each treatment. In addition, small RNA sequencing was carried out on paternal sperm samples to investigate whether long-term psychological stress affected the enrichment of certain sncRNAs and to identify whether they participated in mediating the occurrence and paternal inheritance of the stress-induced DMRs Rsults: Using an optimized data analysis workflow, we obtained approximately 800 million clean reads per sample (build mm10) with strand-specific coverage ~21×, and the data covered ~96.00% of the total 21,867,837 reference CpG dinucleotides. A total of 24,427, 7,975, and 5,173 differentially methylated regions (DMRs) between control and stress groups were found in the F0, F1, and F2 generations, respectively. Inter- and transgenerational inheritance of paternal DMRs were at frequencies approximately 11.36% and 0.48%, respectively. These DMRs related to genes with functional implications for psychological stress response, and tissue inheritance of these DMRs passed paternal disorders epigenetically to offspring. More importantly, these DMRs evaded offspring embryonic reprogramming through erasure and subsequent reestablishment, but not via un-erasure way. Nonetheless, their reestablishment proportions in the primitive streak (E7.5) stage were altered. Furthermore, sncRNA-seq revealed that stress-induced tsRNA, miRNA and rsRNA dysregulation in paternal sperm might play important roles in DMRs occurrence and paternal inheritance.
2021-10-11 | GSE185579 | GEO
Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq, and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice fed with control diet or low-protein diet. We performed expression array analysis to identidy genes which expressions are affected by paternal diet and ATF7 mutation.
2020-03-09 | GSE123251 | GEO
Project description:Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it remains unclear whether phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a specific ligand-receptor interaction and thereby enable pharmacological interrogation of the offspring phenotype, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that paternal exposure to chronic nicotine induced a broad protective response to xenobiotic exposure in the next generation. This effect manifested as increased survival following an injection of toxic levels of nicotine, was specific to male offspring, and was only observed after these offspring were first acclimated to low levels of nicotine for a week. Importantly, offspring xenobiotic resistance was documented not only for toxic nicotine challenge, but also for toxic cocaine challenge, indicating that paternal nicotine exposure reprograms offspring to become broadly resistant to environmental toxins. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, and we found that isolated hepatocytes displayed upregulation of enzymes that metabolize xenobiotics. Taken together, our data show that paternal nicotine exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment.
2017-02-02 | GSE92240 | GEO
Project description:Increasing evidences indicate diet-induced metabolic disorder could be paternally inherited, but the exact sperm epigenetic carrier remains unclear. Here, in a paternal high-fat diet (HFD) mouse model, we revealed that a highly enriched subset of sperm small RNAs (30-34 nt) that derived from the 5â halves of tRNAs (tsRNAs), exhibit changes in both expression profiles and RNA modifications. Injection of sperm tsRNAs from HFD male but not synthetic tsRNAs lacking RNA modifications, into normal zygotes generated metabolic disorders in the F1 offspring. Injection of HFD sperm tsRNAs derails gene expression in both early embryos and islets of F1 offspring, enriched in metabolic pathways, but unrelated to DNA methylation at CpG-enriched region. Collectively, we uncover sperm tsRNAs as a type of âepigenetic carrierâ that mediate intergenerational inheritance of acquired traits. Mature sperm small-RNA profiles between High-fat-diet (HFD) and Normal-diet (ND) males; Transcriptional profiles of 8-cell embryos and balstocysts that developed from zygotes that injected with sperm RNAs from HFD vs ND males. Transcriptional profiles and RRBS profiles of islets of F1 offsrping that generated from zygotes that injected with sperm RNAs from HFD vs ND males.
2015-12-31 | E-GEOD-75544 | biostudies-arrayexpress