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Ancestral folate promotes neuronal regeneration in serial generations of progeny [RNA-seq]

ABSTRACT: Ancestral folate promotes neuronal regeneration in serial generations of progeny [RNA-seq]

PROVIDER: PRJNA566141 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10136830_1.fastq.gz	Fastqsanger.gz
	SRR10136830_2.fastq.gz	Fastqsanger.gz
	SRR10136831_1.fastq.gz	Fastqsanger.gz
	SRR10136831_2.fastq.gz	Fastqsanger.gz
	SRR10136832_1.fastq.gz	Fastqsanger.gz

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Ancestral Folate Promotes Neuronal Regeneration in Serial Generations of Progeny [MeDIP]

Project description:Ancestral folate promotes neuronal regeneration in serial generations of progeny, eliciting transgenerational disruptions in DNA methylation.

2020-03-01 | GSE137642 | GEO

Ancestral folate promotes neuronal regeneration in serial generations of progeny

Project description:Ancestral folate promotes neuronal regeneration in serial generations of progeny

| PRJNA566136 | ENA

Ancestral Folate Promotes Neuronal Regeneration in Serial Generations of Progeny [MeDIP]

Project description:Ancestral Folate Promotes Neuronal Regeneration in Serial Generations of Progeny [MeDIP]

| PRJNA566140 | ENA

Ancestral folate promotes neuronal regeneration in serial generations of progeny [RNA-seq]

Project description:Folate supplementation in F0 mating rodents increases regeneration of injured spinal axons in vivo in at least 4 generations of progeny (F1-F4) in the absence of interval folate administration to the progeny. Transmission of the enhanced regeneration phenotype to untreated progeny parallels axonal growth in neuron culture after in vivo folate administration to the F0 ancestors alone, in correlation with transformed patterns of genomic DNA methylation and gene expression in treated lineages. Enhanced axonal regeneration phenotypes are observed with diverse folate preparations and routes of administration, in outbred and inbred rodent strains, in distinct rodent genera, and are reversed in F4-F5 progeny by pretreatment with DNA demethylating agents prior to phenotyping. Uniform transmission of the phenotype to progeny suggests a non-Mendelian mechanism. The capacity of an essential nutritional co-factor to induce a beneficial transgenerational phenotype in untreated offspring carries broad implications for the diagnosis, prevention, and treatment of inborn and acquired disorders.

2020-03-01 | GSE137641 | GEO

Ancestral Folate Promotes Neuronal Regeneration in Serial Generations of Progeny.

Project description:Folate supplementation in F0 mating rodents increases regeneration of injured spinal axons in vivo in 4 or more generations of progeny (F1-F4) in the absence of interval folate administration to the progeny. Transmission of the enhanced regeneration phenotype to untreated progeny parallels axonal growth in neuron culture after in vivo folate administration to the F0 ancestors alone, in correlation with differential patterns of genomic DNA methylation and RNA transcription in treated lineages. Enhanced axonal regeneration phenotypes are observed with diverse folate preparations and routes of administration, in outbred and inbred rodent strains, and in two rodent genera comprising rats and mice, and are reversed in F4-F5 progeny by pretreatment with DNA demethylating agents prior to phenotyping. Uniform transmission of the enhanced regeneration phenotype to progeny together with differential patterns of DNA methylation and RNA expression is consistent with a non-Mendelian mechanism. The capacity of an essential nutritional co-factor to induce a beneficial transgenerational phenotype in untreated offspring carries broad implications for the diagnosis, prevention, and treatment of inborn and acquired disorders.

| S-EPMC7125003 | biostudies-literature

Ancestral folate promotes neuronal regeneration in serial generations of progeny

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-01 | GSE137643 | GEO

Placenta insufficiency caused by abnormal folate metabolism linked to fetal growth restriction across gestation and generations [RNA-Seq]

Project description:Folate is important for fetal development and growth, yet its role in placentation is understudied. Here we report that disrupting folate metabolism by the hypomorphic Mtrr mutation in mice causes morphological and functional defects in their placentas that correspond with early- and late-onset fetal growth restriction. Remarkably, Mtrr heterozygous males initiate inheritance of similar placenta phenotypes and fetal growth defects in their wildtype grandprogeny. An integrated genome-wide approach shows placental transcriptional change and epigenetic instability is caused by an intrinsic or ancestral Mtrr mutation, affecting genes important for placenta development and function (e.g., pregnancy specific glycoprotein (Psg)/Ceacams). Crucially, we establish a functional association between mouse placenta transcript levels and fetal size and identify a human PSG gene variant linked to birthweight. This study provides molecular insight into how folate metabolism influences placental development and attributes a potential multigenerational epigenetic mechanism to unexplained cases of fetal growth defects.

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Gene expression changes in response to ancestral maternal obesity

Project description:Maternal obesity can program offspring metabolism across multiple generations. It is not known whether multigenerational effects reflect true inheritance of the induced phenotype, or are due to serial propagation of the phenotype through repeated exposure to a compromised gestational milieu. Here we sought to distinguish these possibilities, using the Avy mouse model of maternal obesity. In this model, F1 sons of obese dams display a predisposition to hepatic insulin resistance which remains latent unless the offspring are challenged with a Western diet. We find that F2 grandsons and F3 great-grandsons of obese dams also carry the latent predisposition to metabolic dysfunction, but remain metabolically normal on a healthy diet. Given that the breeding animals giving rise to F2 and F3 were maintained on a healthy diet, the latency of the phenotype permits exclusion of serial programming; we also confirmed that F1 females remained metabolically healthy during pregnancy. Molecular analyses of male descendants identified upregulation of hepatic Apoa4 as a consistent signature of the latent phenotype across all generations. Our results exclude serial programming as a factor in transmission of the metabolic phenotype induced by ancestral maternal obesity, and indicate inheritance through the germline, probably via some form of epigenetic inheritance.

2017-10-01 | GSE103786 | GEO

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Environmental Pollutant Induced Epigenetic Predisposition to Developmental Defects and Cancer Phenotypes in the Progeny

Project description:Hexavalent Chromium, Cr(VI), exposure is known to cause cancer and is a significant human health concern. While the effect of Cr(VI) exposure on exposed individuals is well studied, long-term effects of the same on the progeny of exposed individual are not known. In this study, using Drosophila model system, we show that Cr(VI) exposure of mothers leads to phenotypic variations in the progeny who have never been exposed to Cr(VI). These phenotypic variations arise due to epigenetic instability in the somatic tissues of the progeny rather than novel genetic mutations. Using a Drosophila cancer model system, we also show that maternal Cr(VI) exposure can lead to cancer phenotypes in the progeny and the propensity to cause cancer phenotypes in the progeny is fixed in the population for at least three generations. Thus, we show for the first time that effects of Cr(VI) exposure can last for several generations. This study also lays the foundation to use Drosophila model system to provide novel insights into Cr(VI) and other heavy metal toxicity.

2019-01-01 | GSE111834 | GEO

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