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CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing [smallRNA-seq]

ABSTRACT: CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing [smallRNA-seq]

PROVIDER: PRJNA733154 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14667312.fastq.gz	Fastqsanger.gz
	SRR14667313.fastq.gz	Fastqsanger.gz
	SRR14667314.fastq.gz	Fastqsanger.gz
	SRR14667315.fastq.gz	Fastqsanger.gz
	SRR14667316.fastq.gz	Fastqsanger.gz

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CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing

Project description:CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing

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Project description:CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing [RNA-seq]

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CAG repeat expansion in the Huntington’s Disease gene correlates with defective linear and back-splicing

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Project description:Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. There is no cure for HD, existing pharmaceutical can only relieve its symptoms. Here, induced pluripotent stem cells were established from patients with low CAG repeat expansion in the huntingtin gene, and were then efficiently differentiated into GABA MS-like neurons under defined culture conditions. Analysis of differentially expressed genes between Huntington’s disease and wild type iPSCs derived GABA MS-like neurons has been performed.

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A broad phenotypic screen identifies novel dominant phenotypes in Huntington’s disease CAG knock-in mice

Project description:Huntington’s disease (HD) is a dominantly inherited neurodegenerative disorder characterized by abnormal voluntary and involuntary movements, cognitive impairment and psychiatric disturbances. In order to identify phenotypic changes in the mouse that are most likely to be relevant to events triggered by the CAG repeat expansion in HD patients, we are interested in the earliest events that are triggered by expression of a single allele’s worth of full-length mutant huntingtin in the mouse, whether at the molecular, cellular or whole animal level. To this end, we have undertaken a broad-based, unbiased phenotypic screen in heterozygous HdhQ111/+ C57BL/6J mice. For expression profiling analysis, four male mice at the age of 18 weeks were analysed versus a pool of four male wildtype mice (reference) at the same age. For each single mouse, two chip hybridizations, including a dye-swap experiment, were performed per tissue. Using our genome-wide microarray platform, we performed transcriptome analysis of liver and brain.

2011-09-30 | E-GEOD-28232 | biostudies-arrayexpress

Project description:Huntington’s disease (HD) is a devastating disease for which currently no therapy is available. It is a progressive autosomal dominant neurodegenerative disorder that is caused by a CAG repeat expansion in the HD gene, resulting in an expansion of polyglutamines at the N-terminal end of the encoded protein, designated huntingtin, and the accumulation of cytoplasmic and nuclear aggregates. Not only is there a loss of normal huntingtin function, upon expansion of the CAG repeat there is also a gain of toxic function of the huntingtin protein and this affects a wide range of cellular processes. To identify groups of genes that could play a role in the pathology of Huntington’s disease, we studied mRNA changes in an inducible PC12 model of Huntington’s disease before and after aggregates became visible. This is the first study to show the involvement Nrf2-responsive genes in the oxidative stress response in HD. Oxidative stress related transcripts were altered in expression suggesting a protective response in cells expressing mutant huntingtin at an early stage of cellular pathology. Furthermore, there was a down-regulation of catecholamine biosynthesis resulting in lower dopamine levels in culture. Our results further demonstrate an early impairment of transcription, the cytoskeleton, ion channels and receptors. Given the pathogenic impact of oxidative stress and neuroinflammation, the Nrf2-ARE signaling pathway is an attractive therapeutic target for neurodegenerative diseases. Keywords: Gene expression analysis, Huntington's disease, oxidative stress, PC12 cell model

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