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Ancestral Folate Promotes Neuronal Regeneration in Serial Generations of Progeny.

ABSTRACT: 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.

SUBMITTER: Patel NJ

PROVIDER: S-EPMC7125003 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Ancestral folate promotes neuronal regeneration in serial generations of progeny

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

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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 [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.

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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]

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

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

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Current progress of mitochondrial transplantation that promotes neuronal regeneration.

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Chronic Gestational Inflammation: Transfer of Maternal Adaptation over Two Generations of Progeny.

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| S-EPMC6754931 | biostudies-literature

Fitness Consequences of Advanced Ancestral Age over Three Generations in Humans.

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The cellular prion protein promotes neuronal regeneration after acute nasotoxic injury.

Project description:Adult neurogenesis, analogous to early development, is comprised of several, often concomitant, processes including proliferation, differentiation, and formation of synaptic connections. However, due to continual, asynchronous turn-over, newly-born adult olfactory sensory neurons (OSNs) must integrate into existing circuitry. Additionally, OSNs express high levels of cellular prion protein (PrPC), particularly in the axon, which implies a role in this cell type. The cellular prion has been shown to be important for proper adult OSN neurogenesis primarily by stabilizing mature olfactory neurons within this circuitry. However, the role of PrPC on each specific adult neurogenic processes remains to be investigated in detail. To tease out the subtle effects of prion protein expression level, a large population of regenerating neurons must be investigated. The thyroid drug methimazole (MTZ) causes nearly complete OSN loss in rodents and is used as a model of acute olfactory injury, providing a mechanism to induce synchronized OSN regeneration. This study investigated the effect of PrPC on adult neurogenesis after acute nasotoxic injury. Altered PrPC levels affected olfactory sensory epithelial (OSE) regeneration, cell proliferation, and differentiation. Attempts to investigate the role of PrPC level on axon regeneration did not support previous studies, and glomerular targeting did not recover to vehicle-treated levels, even by 20 weeks. Together, these studies demonstrate that the cellular prion protein is critical for regeneration of neurons, whereby increased PrPC levels promote early neurogenesis, and that lack of PrPC delays the regeneration of this tissue after acute injury.

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