MiRNA-seq for WT and R6/2 (HD) mice with Translin-associated protein X (TRAX) knockdown
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA777623 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16764951.fastq.gz | Fastqsanger.gz | |||
| SRR16764952.fastq.gz | Fastqsanger.gz | |||
| SRR16764953.fastq.gz | Fastqsanger.gz | |||
| SRR16764954.fastq.gz | Fastqsanger.gz | |||
| SRR16764955.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq for WT and R6/2 (HD) mice with Translin-associated protein X (TRAX) knockdown
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Project description:The miRNA/mRNA regulation by Translin associated factor X (TRAX) in WT and R6/2 HD mice
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2011-10-12 | E-GEOD-1980 | biostudies-arrayexpress
Project description:RNA interference is required to form the centromeric heterochromatin needed for chromosome segregation fidelity. Central to this is Argonaute protein, which processes small interfering RNAs (siRNAs) within a self-enforcing feedback mechanism that utilizes the guidance of siRNAs to nucleate heterochromatin-mediators. siRNA processing by Argonaute-containing complexes is enhanced by Translin and Trax proteins. Current dogma purports that impairment of Argonaute drives centromeric heterochromatin dysregulation and chromosome instability. We used the fission yeast to demonstrate that loss of Trax can suppress the chromosomal instability conferred by loss of Argonaute in a Translin-dependent fashion, without restoring centromeric heterochromatin. Extended analysis of Trax and Translin defective cells revealed a conserved role for Trax and Translin in telomeric transcription. This not only identified a novel telomere regulatory activity, but also demonstrates that under conditions of centromeric dysfunction telomeric transcriptional stasis can negatively impact chromosome segregation.
2016-12-01 | GSE71983 | GEO
Project description:HD R6/1 transgenic mouse line brain hemispheres dissected. RNA targets were created for transgenics and wildtypes at time points 18, 22 and 27 weeks. Profiles and data analysis performed using the Bioconductor software and linear model contrasts using LIMMA on RMA probeset summarys. Experiment Overall Design: 18 samples extracted, 3 transgenic plus 3 littermate controls analysed at each timepoint.
2009-04-23 | E-GEOD-3621 | biostudies-arrayexpress
Project description:The endogenous RNA substrates of Translin-TRAX complexes (also known as C3POs) and how they regulate diverse biological processes remain unknown. Here we show that Translin and TRAX do not play a significant role in RNAi in the filamentous fungus Neurospora crassa. Instead, the Neurospora C3PO complex functions as a ribonuclease that removes the 5M-bM-^@M-^Y pre-tRNA fragments after the processing of pre-tRNAs by RNase P. In translin and trax mutants, 5M-bM-^@M-^Y pre-tRNA fragments accumulate to very high levels that can be degraded specifically by both recombinant and endogenous Neurospora C3PO and recombinant Drosophila C3PO. In addition, the mutants have elevated tRNA levels and increased levels of protein translation and are more resistant to a programmed cell-death inducing agent. Together, this study identified the endogenous RNA substrates of C3PO and provides a potential explanation for its roles in seemingly diverse biological processes. Examine small RNA population changes in two different strain background
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Project description:For the bilateral intrastriatal delivery of AAV expressing control or TRAX shRNA, mice were anesthetized with ketamine/xylazine HCl (87.56 and 7.5 ug/kg, respectively, via an intraperitoneal injection) and injected with the indicated AAV (2 µl per injection spot, 2.5*10^9 vector genome/µl) with a 10 ml syringe (Hamilton, Reno, NV, USA) at a rate of 0.5 ul/min. The AAV was injected at the desired position: AP+0.5, L±2, DV-2.5 and -3.5 mm relative to bregma and the dura surface. Then the mouse brains were removed from the mice directly for dissection of striatum. RNA was extracted by TRIzol reagent or miRNeasy mini kit (Qiagen). DNase digestion was performed by the DNA-free™ Kit (Life Technologies, Carlsbad, CA, USA) or the RNase-free DNase set (Qiagen) following the manufacturer’s instructions. The concentration and purity of RNA were measured at 260, 280 and 230 nm by a NanoDrop (Thermo Fisher Scientific, Waltham, MA, USA). Sample libraries were prepared using the QIAseq miRNA Library Kit (QIAGEN) according to the manufacturer's protocols. Adaptors are ligated sequentially to the 3' and 5' ends of miRNAs. Subsequently, universal cDNA synthesis with UMI assignment, cDNA cleanup, library amplification and library cleanup are performed. Libraries were sequenced on an Illumina instrument (75-cycle single-end read, 75SE). Sequencing data was processed using the Illumina software BCL2FASTQ v2.20. Initially, the sequences generated went through a filtering process to obtain qualified reads. Trimmomatic (1) was implemented to clip the 3′ adaptor sequence, trim or remove the reads according to the quality score and discard trimmed reads shorter than 18 nucleotides. Qualified reads after filtering low-quality data were analyzed using miRDeep2 (2) for aligning reads to the reference genome downloaded from UCSC. Only reads that mapped perfectly to the genome five or less times were used for miRNA detection, since miRNAs usually map to few genomic locations. MiRDeep2 estimates expression levels of known miRNAs, and also identifies novel miRNAs. The small RNA library construction, NGS deep sequencing and bioinformatic analysis were accomplished by Welgene Biotech. Co., Ltd. (Taipei, ROC).
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Project description:Animal models play a critical role in the study of Huntington’s disease (HD), for example to elucidate underlying molecular mechanisms or to develop novel therapeutic venues. One of the first transgenic mouse models of HD, the R6/2 line, has been described in 1996 and has since become one of the most studied models of the disease (Mangiarini et al. 1996; Li, Popovic & Brundin 2005). R6/2 mice express the human exon 1 under control of the human huntingtin promoter at around 75% of the endogenous levels. The expression of the exon 1 with a CAG repeat length of around 115 evokes rapid disease progression and animals display multiple HD-associated neuropathological changes. First signs of disease can occur as early as three weeks and mice are severely impaired by the age of 8-12 weeks. The expected life span is 13-16 weeks (Li, Popovic & Brundin 2005). Here we were interested in the changes occurring in the proteomic landscape as well as in phosphoproteomic signaling networks in the R6/2 mouse model as compared to wild type mice. To this end, we performed comprehensive quantitative phosphoproteome and proteome analyses of striatum of one, two, and three months old mice of both genotypes. A total of nine or more samples per group was analyzed according to the experimental layout shown above. To allow for accurate quantification, peptides of each sample were labelled using tandem mass tags (TMT) and replicates of different conditions were combined. Each combined sample contained an aliquot of a pooled sample consisting of 12 sample lysates. This pooled sample was intended to serve as a reference to allow for quantitative comparison between all combined samples.
2019-06-03 | PXD013771 | Pride
Project description:Huntington’s disease is a genetic disease caused by a single mutation. It is characterised by progressive movement, emotional and cognitive deficits. R6/2 transgenic mice carrying the Huntington’s disease mutation have a progressive neurological phenotype, including deterioration in cognitive function. The mechanism underlying the cognitive deficits in R6/2 mice is unknown, but dysregulated gene expression, reduced neurotransmitter levels and abnormal synaptic function are present before the cognitive decline becomes pronounced. Our goal here was to ameliorate the cognitive phenotype in R6/2 mice using a combination drug therapy (tacrine, moclobemide and creatine) aimed boosting neurotransmitter levels in the brain. Treatment from 5 weeks of age prevented deterioration in two different cognitive tasks until at least 12 weeks. However, motor deterioration continued unabated. Microarray analysis of global gene expression revealed that many genes significantly up- or down-regulated in untreated R6/2 mice had returned towards normal levels after treatment. Thus dysregulated gene expression was reversed by the combination treatment in the R6/2 mice and probably underlies the observed improvements in cognitive function. Our study shows that cognitive decline caused by a genetic mutation can be slowed by a combination drug treatment, and gives hope that cognitive symptoms in HD can be treated. Keywords = HD Keywords = Huntingtin Keywords = cognitive disorder Keywords = R6/2 Keywords = transgenic mice Keywords = gene expression Keywords = microarray Keywords: ordered
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