Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20644638.fastq.gz | Fastqsanger.gz |
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Project description:PURPOSE: The transcriptional repressor PARIS (ZNF746) was initially identified as a pathogenic co-substrate of PINK1 and parkin that leads to Parkinson’s disease (PD) by disrupting mitochondrial biogenesis through PPARγ coactivator -1α (PGC-1α) suppression. Later, accumulation of PARIS in dopamine (DA) neurons that cause neurotoxicity has been studied widely and growing evidence has linked defective mitochondrial biogenesis to PD pathogenesis. Yet, the mechanistic underpinnings of this link remain elusive. METHODS: We performed a global, model-based analysis of PARIS genomic occupancy using chromatin immune-precipitation followed by sequencing (ChIP-seq) on SHSY-5Y in human cell line. The dataset is composed of PARIS and control samples, each with one replicate only. For each sample, after quality control as mentioned above, reads were separately aligned to the latest human genome (NCBI; GRCh38) using Bowtie with the parameter “-m 1” to retain uniquely mapped reads only. The R packages ChIPQC v1.20.0 and PhantomPeakQualTools v1.2.2 were used to confirm the quality of the aligned bam files based on the ChIP-seq guidelines by ENCODE consortium (NSC >= 1.05; RSC >= 0.8, Qtag={-2,-1,0,1,2}). QC-confirmed bam files were subject to differential peak calling using MACS v1.4.220 with the following parameters: -t Sample.sam -c Control.sam --format SAM -g hs -B -S --call-subpeaks. Peak annotation and visualization were done using the R packages ChIPseeker v1.20.0 and clusterProfiler v3.12.0, respectively. RESULTS: We showed that PPARγ acts as a master regulator of transcriptomic changes induced by PARIS in the clusters of Drosophila dopaminergic neurons. Also, we revealed that PARIS directly modulates expression of PPARγ target genes by physically binding to the promoter regions. And finally, we observed a PARIS binding motif at the promoter proximal site of PPARγ, implying a direct regulatory effect of PARIS on PPARγ expression profile. CONCLUSION: PARIS displays adverse effects on modulation of PPARγ associated gene clusters. Our work revealed a pivotal role of PPARγ in PARIS-driven neurodegeneration.
2021-08-02 | GSE175555 | GEO
Project description:Paris sp. CG-2021b Genome sequencing and assembly
| PRJNA861440 | ENA
Project description:PURPOSE: The transcriptional repressor PARIS (ZNF746) was initially identified as a pathogenic co-substrate of PINK1 and parkin that leads to Parkinson’s disease (PD) by disrupting mitochondrial biogenesis through PPARγ coactivator -1α (PGC-1α) suppression. Later, accumulation of PARIS in dopamine (DA) neurons that cause neurotoxicity has been studied widely and growing evidence has linked defective mitochondrial biogenesis to PD pathogenesis. Yet, the mechanistic underpinnings of this link remain elusive. METHODS: We employed translating ribosome affinity purification (TRAP) followed by RNA sequencing (TRAP-seq) for transcriptome profiling of DA neurons in transgenic Drosophila lines we generated expressing human PARIS or human PARIS mutant (C571A). Together with TRAP control and whole brain samples, this data set is composed of a total of 10 (3, 3, 3, and 1 respectively) replicate samples representing 4 different treatment groups for a set of gene-level (a parametric F-test) and transcript-level (a Wald test or a likelihood ratio test) differential expression analysis. RESULTS: Firstly, we identified differentially expressed genes by human PARIS in fly DA neurons successfully. Then, we showed that PPARγ acts as a master regulator of transcriptomic changes induced by PARIS in the clusters of Drosophila dopaminergic neurons. Also, we validated this finding in human neuroblastoma cell line. CONCLUSION: PPARγ plays a crucial regulatory role in PARIS phenotype. Drosophila models of PARIS-induced neurodegeneration used in this work to represent PD phenotype and our TRAP-seq protocol serve as a paradigm for future studies to unravel mechanistic underpinnings of PARIS biology.
2021-08-02 | GSE175554 | GEO
Project description:Paris polyphylla Genome sequencing and assembly
| PRJNA815456 | ENA