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Effect of frataxin silencing by RNAi on 4, 7 and 14 days old worms

ABSTRACT: Effect of frataxin silencing by RNAi on 4, 7 and 14 days old worms

PROVIDER: PRJNA937591 | ENA |

REPOSITORIES: ENA

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Effect of frataxin silencing by RNAi on 4, 7 and 14 days old worms

Project description:The study aimed to investigate the mechanisms that promote compensatory pro-longevity responses during mild mitochondrial stress in Caenorhabditis elegans. This was achieved by performing a DNA microarray analysis to compare gene expression profiles of wild-type and mild mitochondrial-stressed long-lived worms at days 4, 7, and 14 after birth, in five replicates. The worms were fed with either an empty-vector control (pL4440) or vector-expressing dsRNA against nematode frataxin (frh-1) to induce mild mitochondrial stress, for 3 consecutive generation starting from eggs.

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C. elegans total RNA profiles of worms treated with RNAi for different Integrator complex

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42 days old adult worms: adult worms vs. adult worms (self-self)

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2007-12-20 | GSE6915 | GEO

Proteomics after co-immunoprecipitation of myosin/MHC B/UNC-54 (with a Gly387Arg mutation) from C. elegans worms grown on nhl-1 or F40A3.6 RNAi compared to control RNAi

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mRNA-seq of worms who raised on control RNAi or prp-19 RNAi were untreated or treated with atp-2 RNAi

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Functional genomic analysis of frataxin deficiency, Illumina data

Project description:Functional genomic analysis of frataxin deficiency reveals tissue-specific alterations and identifies the PPARÎ³ pathway as a therapeutic target in Friedreich's ataxia Friedreich's ataxia (FRDA), the most common inherited ataxia, is characterized by focal neurodegeneration, diabetes mellitus, and life-threatening cardiomyopathy. Frataxin, which is significantly reduced in patients with this recessive disorder, is a mitochondrial iron-binding protein, but how its deficiency leads to neurodegeneration and metabolic derangements is not known. We performed microarray analysis of heart and skeletal muscle in a mouse model of frataxin deficiency, and found molecular evidence of increased lipogenesis in skeletal muscle, and alteration of fiber-type composition in heart, consistent with insulin resistance and cardiomyopathy, respectively. Since the peroxisome proliferator-activated receptor gamma (PPARÎ³) pathway is known to regulate both processes, we hypothesized that dysregulation of this pathway could play a key role in frataxin deficiency. We confirmed this by showing a coordinate dysregulation of the PPARÎ³ coactivator Pgc1a and transcription factor Srebp1 in cellular and animal models of frataxin deficiency, and in cells from FRDA patients, who have marked insulin resistance. Finally, we show that genetic modulation of the PPARÎ³ pathway affects frataxin levels in vitro, supporting PPARÎ³ as a novel therapeutic target in FRDA. To compare frataxin deficient (KIKO) mice vs. WT, heart, skeletal muscle, and liver.

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