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ChIPseq on bulk striatal tissue of 15-20 week-old HD R6/1 mice

ABSTRACT: ChIPseq on bulk striatal tissue of 15-20 week-old HD R6/1 mice

PROVIDER: PRJNA1090133 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28400300.fastq.gz	Fastqsanger.gz
	SRR28400293.fastq.gz	Fastqsanger.gz
	SRR28400294.fastq.gz	Fastqsanger.gz
	SRR28400295.fastq.gz	Fastqsanger.gz
	SRR28400296.fastq.gz	Fastqsanger.gz

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ChIPseq on bulk striatal tissue of 15-20 week-old HD R6/1 mice

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Gene expression data from cortex of 9 week old wild type, R6/2, HDAC4het and R6/2::HDAC4het mice

Project description:Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington's disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics. mRNA expression analysis was performed by microarray in 9 weeks old WT (n=9), R6/2 (n=9), HDAC4het (n=9) and Double R6/2::HDAC4het (n=10) mice. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).

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