EGAS00001002861-sc-2020-01-15T09:33:21Z - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001005788 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:We will be testing the hypothesis that MBD4 PTV germline carriers also show an increased number of C toT germline mutations in their offspring.
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAS00001002861 | EGA
Project description:The aim of this project is to use transcriptome sequencing of parents and offspring of Leishmania tropica genetic crosses to establish the basic parameters of recombination in this species and to understand the extent and importance of gene conversion. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-06-25 | E-ERAD-408 | biostudies-arrayexpress
Project description:BRCA1 germline mutation carriers are predisposed to breast cancers. Epigenomic regulations have been known to strongly interact with genetic variations and potentially mediate biochemical cascades involved in tumorigenesis. Due to the cell-type specificity of epigenomic features, profiling of individual cell types is critical for understanding the molecular events in various cellular compartments within complex breast tissue. Here we report cell-type specific profiling of genome-wide histone modifications, including H3K27ac and H3K4me3 in basal, luminal progenitor, mature luminal, and stromal cells, extracted from pre-cancer BRCA1 mutation carriers and non-carriers, using a low-input technology. We discover that basal and stromal cells present the most substantial epigenomic differences between mutation carriers and non-carriers while luminal progenitor and mature luminal cells are relatively unchanged with the mutation. Furthermore, the epigenomic changes in basal cells due to BRCA1 mutation appear to facilitate their transformation into luminal progenitor cells. Our findings shed light on the pre-cancer epigenomic dynamics due to BRCA1 mutation and how they may contribute to eventual development of basal-like breast cancer.
2020-08-25 | GSE148995 | GEO
Project description:Investigation of genome-wide germline copy number mutations in mice after parental exposure to 3 Gy of acute X-rays The level of copy number mutations in offspring of exposed paternal mice was substantially increased when compared to the control Overall 262 samples were used of which 93 were control samples and 169 treated samples. The control samples came from offspring of parents (C57BL6/J (male) and CBA/Ca (female)) with sham -ir while the treated samples were from offspring of 3 Gy whole-body acute irradiated paternal and non-exposed maternal. The treated samples classified into two groups: post-meiotic and pre-meiotic according to exposed status of the sperm that gave rise to the offspring. The reference sample for each offspring was equal mixture of paternal and maternal DNA.
2015-02-04 | E-GEOD-65521 | biostudies-arrayexpress
Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is unexplored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>
2024-02-12 | MTBLS1629 | MetaboLights
Project description:Bottleneck sequencing of human tissue including neurons, cord blood, sperm.
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ .
This dataset contains all the data available for this study on 2020-10-20.
| EGAD00001006459 | EGA
Project description:T-cell clones were obtained by limiting dilution culture of PBMC of HTLV-1 carriers. Exon expression profiling was performed using Affymetrix exon array (Affymetrix Human Exon 1.0 ST Array) according to the manufacturer's instructions. Gene version of CEL files 01 to 12 are presented in GSE46518.
2015-11-01 | GSE52244 | GEO
Project description:Tag profiling and expression analysis of genes from Pachycladon enysii and Pachycladon fastigiatum. ArrayExpress Release Date: 2011-06-01 Publication Title: Short read expression profiling in a non-model allopolyploid plant Publication Author List: Voelckel, C, Gruenheit, N, Biggs, P, Deusch, O, Lockhart, PJ Person Roles: submitter Person Last Name: Voelckel Person First Name: Claudia Person Mid Initials: Person Email: c.voelckel@massey.ac.nz Person Phone: Person Address: Institute of Molecular Biosciences, Private Bag 11 222, Palmerston North 4442 Person Affiliation: Institute of Molecular Biosciences, Allan Wilson Centre for Molecular Ecology and Evolution
2011-07-14 | GSE30618 | GEO
Project description:Traditional research has focused on DNA as the molecule that carries heritable information from the parent to the offspring. However, increasing evidence suggests that information beyond the DNA sequence, termed epigenetic information, can also transmit certain information from one generation to the next. Whereas paternal epigenetic germline inheritance has been well elucidated, as the father contributes little more than a sperm cell to the offspring, maternal epigenetic inheritance via gametes remains largely unclear. Here, using an in vitro fertilization system and a micromanipulation strategy, we demonstrate that oocyte piRNAs mediate intergenerational transmission of an acquired metabolic disorder. Changes in the expression profiles of many oocyte piRNAs are observed in a maternal chronic high-fat diet (HFD) mouse model. Injection of the oocyte piRNAs from HFD females into normal zygotes resulted in impaired glucose tolerance and decreased insulin sensitivity in the F1 offspring. A series of genes involved in glucose metabolism and the insulin signaling pathway were differentially expressed in the pancreatic islets of the F1 offspring. Bisulfite genome sequencing of the islets of the F1 offspring revealed changes in cytosine methylation that correlated with the observed gene expression patterns. These data identified oocyte piRNAs as novel carriers of epigenetic information and highlight the importance of long-term maternal health before conception.
2021-05-17 | GSE174504 | GEO
Project description:Background: Non-genetic disease inheritance and offspring phenotype is substantially influenced by germline epigenetic programming, including genomic imprinting. Loss of Polycomb Repressive Complex 2 (PRC2) function in oocytes causes non-genetically inherited effects on offspring, including embryonic growth restriction followed by post-natal offspring overgrowth. While PRC2 dependent non-canonical imprinting is likely to contribute, less is known about germline epigenetic programming of non-imprinted genes during oocyte growth. In addition, de novo germline mutations in genes encoding PRC2 lead to overgrowth syndromes in human patients, but the extent to which PRC2 activity is conserved in human oocytes is poorly understood. Results: In this study we identify a discrete period of early oocyte growth during which PRC2 is expressed in mouse growing oocytes. Deletion of Eed during this window led to the de-repression of 343 genes. A high proportion of these were developmental regulators, and the vast majority were not imprinted genes. Many of the de-repressed genes were also marked by the PRC2-dependent epigenetic modification histone 3 lysine 27 trimethylation (H3K27me3) in primary-secondary mouse oocytes, at a time concurrent with PRC2 expression. In addition, we found H3K27me3 was also enriched on many of these genes by the germinal vesicle (GV) stage in human oocytes, strongly indicating that this PRC2 function is conserved in the human germline. However, while the 343 genes were de-repressed in mouse oocytes lacking EED, they were not de-repressed in pre-implantation embryos and lost H3K27me3 during pre-implantation development. This implies that H3K27me3 is a transient feature that represses a wide range of genes in oocytes. Conclusions: Together, these data indicate that EED has spatially and temporally distinct functions in the female germline to repress a wide range of developmentally important genes, and that this activity is conserved in the mouse and human germlines.
2023-01-11 | GSE193582 | GEO