Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The microbiota and T cells non-genetically modulate inherited phenotypes transgenerationally

ABSTRACT: The microbiota and T cells non-genetically modulate inherited phenotypes transgenerationally

PROVIDER: PRJNA1005268 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25634400_1.fastq.gz	Fastqsanger.gz
	SRR25634400_2.fastq.gz	Fastqsanger.gz
	SRR25634500_1.fastq.gz	Fastqsanger.gz
	SRR25634500_2.fastq.gz	Fastqsanger.gz
	SRR25634600_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 409

Similar Datasets

The microbiota and T cells non-genetically modulate inherited phenotypes transgenerationally

Project description:The host-microbiota relationship has evolved to shape mammalian physiology, including immunity, metabolism, and development. Germ-free models are widely used to study microbial effects on host processes such as immunity. Here, we find that both germ-free and T cell-deficient mice exhibit a robust sebum secretion defect persisting across multiple generations despite microbial colonization and T cell repletion. These phenotypes are inherited by progeny conceived during in vitro fertilization using germ-free sperm and eggs, demonstrating that non-genetic information in the gametes is required for microbial-dependent phenotypic transmission. Accordingly, gene expression in early embryos derived from gametes from germ-free or T-cell deficient mice are strikingly and similarly altered. Our findings demonstrate that microbial and immune-dependent regulation of non-genetic information in the gametes can transmit inherited phenotypes transgenerationally in mice. This mechanism could rapidly generate phenotypic diversity to enhance host adaptation to environmental perturbations.

2024-03-24 | GSE240797 | GEO

Sperm-inherited H3K27me3 epialleles are transmitted transgenerationally in cis

Project description:Sperm-inherited H3K27me3 epialleles are transmitted transgenerationally in cis

| PRJNA843785 | ENA

Sperm-inherited H3K27me3 epialleles are transmitted transgenerationally in cis

Project description:The role that gamete-inherited chromatin states serve in regulating gene expression across generations is poorly understood. To interrogate how histone marks inherited on parental genomes influence gene expression in offspring, we profiled different tissue contexts in worms that inherited the sperm genome lacking the repressive mark H3K27me3. We found that worms that inherited the sperm genome lacking H3K27me3 upregulated genes in all tissues profiled, which included hermaphrodite and male germlines and mixed soma. We found that most upregulated genes were upregulated specifically from sperm alleles and in a tissue-specific manner, highlighting the importance of cellular context in determining which genes are sensitive to upregulation when H3K27me3 repression is absent. To determine whether chromatin states can impact gene expression transgenerationally, i.e. across 3 generations, we profiled gene expression and chromatin states in the germlines of worms that inherited the sperm genome lacking H3K27me3 (F1 generation) and in the germlines of their offspring (F2 generation). We found that genes upregulated in F1 germlines maintained the H3K27me3(-) state of sperm alleles and that the upregulated and H3K27me3(-) state of sperm alleles was maintained in the germlines of their offspring (F2 generation). These findings demonstrate that histone marks can serve as a transgenerational carrier.

2022-05-31 | GSE205113 | GEO

Adipocyte Epigenetic Alterations and Potential Therapeutic Targets in Transgenerationally Inherited Lean and Obese Phenotypes Following Ancestral Exposure to Environmental Toxicants

Project description:Adipocyte Epigenetic Alterations and Potential Therapeutic Targets in Transgenerationally Inherited Lean and Obese Phenotypes Following Ancestral Exposure to Environmental Toxicants

| PRJNA565793 | ENA

Neuronal Small RNAs Control Behavior Transgenerationally

Project description:It is unknown whether the activity of the nervous system can be inherited. In Caenorhabditis elegans nematodes, parental responses can transmit heritable small RNAs that regulate gene expression transgenerationally. In this study we show that a neuronal process can impact the next generations. Neurons-specific synthesis of RDE-4-dependent small RNAs regulates germline amplified endogenous siRNAs and germline gene expression for multiple generations. Further, the production of small RNAs in neurons controls the chemotaxis behavior of the progeny for at least three generations via the germline Argonaute HRDE-1. Among the targets of these small RNAs we identified the conserved gene saeg-2, which is transgenerationally downregulated in the germline. Silencing of saeg-2 following neuronal small RNA biogenesis is required for chemotaxis under stress. Thus, we propose a small RNA-based mechanism for communication of neuronal processes transgenerationally.

2019-06-05 | GSE124049 | GEO

Impaired DNA replication derepresses chromatin and generates a transgenerationally inherited epigenetic memory

Project description:Impaired DNA replication is a hallmark of cancer and a cause of genomic instability. We report that, in addition to causing genetic change, impaired DNA replication during embryonic development can have major epigenetic consequences for a genome. In a genome-wide screen, we identified impaired DNA replication as causing increased expression from a repressed transgene in Caenorhabditis elegans. The acquired expression state behaved as an “epiallele,” being inherited for multiple generations before fully resetting. Derepression was not restricted to the transgene but was caused by a global reduction in heterochromatin-associated histone modifications due to the impaired retention of modified histones on DNA during replication in the early embryo. Impaired DNA replication during development can therefore globally derepress chromatin, creating new intergenerationally inherited epigenetic expression states.

2017-09-15 | GSE95034 | GEO

Adipocyte epigenetic alterations and potential therapeutic targets in transgenerationally inherited lean and obese phenotypes following ancestral exposures.

Project description:The incidence of obesity has increased dramatically over the past two decades with a prevalence of approximately 40% of the adult population within the United States. The current study examines the potential for transgenerational adipocyte (fat cell) epigenetic alterations. Adipocytes were isolated from the gonadal fat pad of the great-grand offspring F3 generation 1-year old rats ancestrally exposed to DDT (dichlorodiphenyltrichloroethane), atrazine, or vehicle control in order to obtain adipocytes for DNA methylation analysis. Observations indicate that there were differential DNA methylated regions (DMRs) in the adipocytes with the lean or obese phenotypes compared to control normal (non-obese or lean) populations. The comparison of epigenetic alterations indicated that there were substantial overlaps between the different treatment lineage groups for both the lean and obese phenotypes. Novel correlated genes and gene pathways associated with DNA methylation were identified, and may aid in the discovery of potential therapeutic targets for metabolic diseases such as obesity. Observations indicate that ancestral exposures during critical windows of development can induce the epigenetic transgenerational inheritance of DNA methylation changes in adipocytes that ultimately may contribute to an altered metabolic phenotype.

| S-EPMC6948971 | biostudies-literature

Adipocyte Epigenetic Alterations and Potential Therapeutic Targets in Transgenerationally Inherited Lean and Obese Phenotypes Following Ancestral Exposure to Environmental Toxicants

Project description:This study examines the transgenerational adipocyte (fat cell) epigenetic alterations in F3 generation obese and lean rats ancestrally exposed to DDT and atrazine. Adipocytes were isolated from the gonadal fat pad of F3 generation 1-year old rats ancestrally exposed to DDT, atrazine, or vehicle control in order to obtain adipocyte DNA for DNA methylation analysis. Observations indicate that there were differential DNA methylated regions (DMRs) in the adipocytes with the lean or obese phenotypes compared to control normal (non-obese or lean) populations. Interestingly, there were epigenetic changes that were distinct when comparing the lean and obese DMRs between the control and exposure lineage groups. DMR gene associations were identified which included common set of genes previously shown to associate with adipocyte pathology. The comparison of epigenetic alterations indicated that there were substantial overlaps between the different treatment lineage groups for both the lean and obese phenotypes. Novel correlated genes and gene pathways associated with DNA methylation were identified, and may aid in the discovery of potential therapeutic targets for metabolic diseases such as obesity.

2019-12-31 | GSE137536 | GEO

Neuronal Small RNAs Control Behavior Transgenerationally

Project description:Neuronal Small RNAs Control Behavior Transgenerationally

| PRJNA510611 | ENA

Autism-linked UBE3A gain-of-function mutation causes interneuron and behavioral phenotypes when inherited maternally or paternally in mice (scRNA-Seq)

Project description:The E3 ubiquitin ligase Ube3a is biallelically expressed in mitotic cells, including neural progenitors and glial cells, raising the possibility that UBE3A gain-of-function mutations might cause neurodevelopmental disorders irrespective of parent-of-origin. To test this possibility, we engineered a mouse line that harbors an autism-linked UBE3A-T485A (T508A in mouse) gain-of-function mutation and evaluated phenotypes in animals that inherited the mutant allele paternally, maternally, or from both parents. We found that both paternally and maternally expressed UBE3A-T485A resulted in elevated UBE3A activity in neural progenitors and glial cells where Ube3a is biallelically expressed. Expression of UBE3A-T485A from the maternal allele, but not the paternal one, led to a persistent elevation of UBE3A activity in postmitotic neurons. Maternal, paternal, or biparental inheritance of the mutant allele promoted embryonic expansion of Zcchc12 lineage interneurons which mature into Sst and Calb2 expressing interneurons, and caused a spectrum of behavioral phenotypes that differed by parent-of-origin. Phenotypes were distinct from those observed in Angelman syndrome model mice that harbor a Ube3a maternal loss-of-function allele. Our study shows that the UBE3A-T485A gain-of-function mutation causes distinct neurodevelopmental phenotypes when inherited maternally or paternally. These findings have clinical implications for a growing number of disease-linked UBE3A gain-of-function mutations.

2023-07-03 | GSE201733 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data