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Identification of the RNA targets of RBM5 and transcriptome analysis of the brain of wild-type and R6/2 (Huntington's disease) mice

ABSTRACT: Identification of the RNA targets of RBM5 and transcriptome analysis of the brain of wild-type and R6/2 (Huntington's disease) mice

PROVIDER: PRJNA777565 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16761728_1.fastq.gz	Fastqsanger.gz
	SRR16761728_2.fastq.gz	Fastqsanger.gz
	SRR16761729_1.fastq.gz	Fastqsanger.gz
	SRR16761729_2.fastq.gz	Fastqsanger.gz
	SRR16761730_1.fastq.gz	Fastqsanger.gz

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Identification of the RNA targets of RBM5 and transcriptome analysis of the brain of wild-type and R6/2 (Huntington's disease) mice

Project description:Using the Cross-linking immuno-precipitation (CLIP) methodology combined with high throughput sequencing analysis, we have identified the RNA targets of the RNA-binding protein RBM5 in the brain of wild-type and R6/2 (Huntington's disease model) adult mice. In parallel, transcriptome analysis was performed by RNA-sequencing using brain samples from the same animals.

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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.

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