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Systemic RNA interference-defective (SID) genes modulate dopaminergic neurodegeneration in C. elegans

ABSTRACT: To investigate mutations in genes involved in the cellular import of dsRNA neuroprotection, we generated a profile of individual genes affected when dsRNA transport is incapacitated and established a foundation for the systemic analysis of their distinct contributions to neuroprotection. We then identified a set of previously unreported neuroprotective proteins using data obtained from RNA-seq.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE205118 | GEO | 2022/08/04

REPOSITORIES: GEO

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Mechanistic impacts of bacterial diet on dopaminergic neurodegeneration in a Caenorhabditis elegans α-synuclein model of Parkinson's disease

Project description:Using distinct mutant strains deficient in key aspects of gene silencing machinery, we provide evidence that neuroprotection appears to stem from dsRNAs that originate from the bacteria themselves, and Systemic RNA Interference Defective (SID) mutants deficient in dsRNA-mediated gene silencing do not allow for neuroprotection from the bacteria. Transcriptomic analysis between worms reared on OP50 and HB101 E. coli for multiple generations in an a-syn background revealed that the primary cellular processes involved in neuroprotection of this nature included but were not limited to endopeptidase activity, transcriptional regulation, calcium ion binding activity, and water channel activity.

2023-05-19 | GSE210005 | GEO

p53 prevents neurodegeneration by regulating synaptic genes

Project description:DNA damage has been implicated in neurodegenerative disorders, including Alzheimer’s disease and other tauopathies, but the consequences of genotoxic stress to postmitotic neurons are poorly understood. Here we demonstrate that p53, a key mediator of the DNA damage response, plays a neuroprotective role in a Drosophila model of tauopathy. Further, through a whole-genome ChIP-chip analysis we identify genes controlled by p53 in postmitotic neurons. We genetically validate a specific pathway, synaptic function, in p53-mediated neuroprotection. We then demonstrate that the control of synaptic genes by p53 is conserved in mammals. Collectively, our results implicate synaptic function as a central target in p53-dependent protection from neurodegeneration. 4 samples: tau vs. control

2015-01-06 | E-GEOD-40418 | biostudies-arrayexpress

p53 prevents neurodegeneration by regulating synaptic genes

2015-01-06 | GSE40418 | GEO

Probiotic Lacticaseibacillus rhamnosus HA-114 suppresses age-dependent neurodegeneration via mitochondrial beta-oxidation

Project description:The human microbiota is believed to influence health. Microbiome dysbiosis may be linked to neurological conditions like Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD). We report the ability of a probiotic bacterial strain in halting neurodegeneration phenotypes. We show that Lacticaseibacillus rhamnosus HA-114 is neuroprotective in C. elegans models of ALS and HD. Our results show that neuroprotection from L. rhamnosus HA-114 is unique from other L. rhamnosus strains, and resides in its fatty acid content. Neuroprotection by L. rhamnosus HA-114 requires acdh-1/ACADSB, kat-1/ACAT1 and elo-6/ELOVL3/6, which are key fatty acid metabolism and mitochondrial b-oxidation genes. Our data suggest that disrupted lipid metabolism contributes to neurodegeneration and that dietary intervention with L. rhamnosus HA-114 restores lipid homeostasis and energy balance through mitochondrial b-oxidation. L. rhamnosus HA-114 is suitable for human consumption opening the possibility of modifying disease progression by dietary intervention.

2021-12-05 | GSE189988 | GEO

Caenorhabditis elegans SID-2 is required for environmental RNA interference.

Project description: Not available

| S-EPMC1965553 | biostudies-literature

Early signs of neurodegeneration in dopaminergic neurons observed in a Drosophila model of Parkinson’s disease

Project description:Parkinson’s disease (PD) is the most common neurodegenerative movement disorder characterized by a progressive loss of dopamine-containing neurons in the Substantia nigra and the presence of so-called Lewy bodies. The mechanisms underlying disease initiation and development are poorly understood and causative therapies are currently not available. In order to gain insights into the molecular signatures of affected neurons during early stages of Parkinson’s disease, we utilized a Drosophila Parkinson model. We applied the pesticide rotenone to induce Parkinson-like phenotypes in the fly and isolated dopamine containing neurons of animals at a presymptomatic disease stage in order to elucidate their transcriptomic characteristics. In these rotenone treated neurons several gene ontologies, including regulation of cell death, were significantly enriched. Moreover, numerous signaling pathways known to be relevant for cell survival were apparently deregulated in these neurons. While the activities of the MAPK/EGFR- and TGF-β-signaling pathways were enhanced, the performance of the Wnt-pathway was dampened, which may be of central importance for their increased propensity to undergo apoptosis. Thus, further studies involving these pathways may provide new insights into the molecular events underlying pathogenesis and may lead to the identification of new targets for neuroprotective interventions.

2015-12-01 | GSE74247 | GEO

High-pressure-sprayed double stranded RNA does not induce RNA interference of a reporter gene

Project description:We report the sRNA profile upon dsRNA spraying on 16C (Nicotiana benthamiana) plants. In this experiment we could detect only the degradation products of the dsRNA, which indicates absence of further processing of the dsRNA by RNAi machinery

2020-12-01 | GSE160110 | GEO

Analysis of the retinal gene expression after hypoxic preconditioning identifies candidate genes for neuroprotection

Project description:Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1α in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. Our data suggest that neuroprotection after hypoxic preconditioning of the retina is the result of the differential expression of a multitude of genes which may act in concert to protect visual cells against a toxic insult. Keywords: hypoxic preconditioning, neuroprotection, transcription-profile, retina

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Disrupted iron homeostasis causes dopaminergic neurodegeneration in mice

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2015-03-11 | E-GEOD-66730 | biostudies-arrayexpress

NMNAT2 Is Downregulated in Glaucomatous RGCs and RGC-Specific Gene Therapy with NMNAT2 Overexpression Rescues Glaucomatous Neurodegeneration and Visual Function

Project description:The lack of neuroprotective treatments for retinal ganglion cells (RGCs) and optic nerve (ON) is a central challenge for glaucoma management. Emerging evidence suggests that redox factor NAD+ decline is a hallmark of aging and neurodegenerative diseases including glaucoma. Supplementation with NAD+ precursors and overexpression of the nicotinamide mononucleotide adenylyltransferase (NMNAT), the key enzyme involved in the NAD+ biosynthetic process, have significant neuroprotection effect on glaucoma. Among the three NMNAT isoforms, only NMNAT2 is enriched in neurons, especially in axons, however, its role in glaucoma is not well studied. Here we present the expression levels of the enzymes that involved in NAD+ metabolism in both naïve and glaucomatous mouse RGCs. Intriguingly, NMNAT2 is the dominant form of NMNATs in RGCs and only its mRNA level, but not NMNAT1 or NMNAT3, is significant decreased in glaucomatous RGCs. We then demonstrated proof-of-principal gene therapy strategy of restoring RGC-specific NMNAT2 and NAD+ levels by AAV2-mediated RGC-specific promoter mSncg-driven long half-life NMNAT2 mutant. This gene therapy strategy is further tested in two optic neuropathy models, traumatic ON crush model and ocular hypertension glaucoma model. RGC-specific NMNAT2 overexpression significantly promotes RGC somata and axons survival and preserves visual function in both models. Our studies suggest that the weaking of NMNAT2 expression in glaucomatous RGCs contributes to detrimental NAD+ decline and that modulating RGC intrinsic NMNAT2 level by AAV2-mSncg vector is a potent gene therapy for glaucomatous neuroprotection.

2021-08-22 | GSE182483 | GEO

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