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Transcriptome profiling in knock-in mouse models of Huntington's disease [striatum cortex liver tissue survey]

ABSTRACT: Transcriptome profiling in knock-in mouse models of Huntington's disease [striatum cortex liver tissue survey]

PROVIDER: PRJNA274981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1794090.fastq.gz	Fastqsanger.gz
	SRR1794100.fastq.gz	Fastqsanger.gz
	SRR1794110.fastq.gz	Fastqsanger.gz
	SRR1794120.fastq.gz	Fastqsanger.gz
	SRR1794130.fastq.gz	Fastqsanger.gz

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3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.

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