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Functional sequestration of MOAG-2/LIR-3 by polyglutamine expansion proteins

ABSTRACT: Functional sequestration of MOAG-2/LIR-3 by polyglutamine expansion proteins

PROVIDER: PRJEB12258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1198060.fastq.gz	Fastqsanger.gz
	ERR1198070.fastq.gz	Fastqsanger.gz
	ERR1198080.fastq.gz	Fastqsanger.gz
	ERR1198061.fastq.gz	Fastqsanger.gz
	ERR1198071.fastq.gz	Fastqsanger.gz

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Functional sequestration of MOAG-2/LIR-3 by polyglutamine expansion proteins

Project description:Transcriptome profiling of Lir3 C.elegans mutants. Larval stage L4 worms were used for RNA isolation from N2 (Bristol), Q40 (polyglutamine model) genetic background; Lir3 and wiltype controls. Experiments were done in triplicates using ribosomal RNA depletion. Libraries were sequenced with 50bp reads on Illumina HiSeq2500 platform

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AR function is altered by polyglutamine expansion and by SUMO

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Project description:Polyglutamine(polyQ) expansion of α1A voltage-dependent calcium channel (Cav2.1) is the causative mutation of spinocerebellar ataxia type 6 (SCA6). The C-terminal fragment (CTF) of Cav2.1 makes aggregates in the cytoplasm of SCA6 Purkinje cells and may relate to the pathogenesis. In order to identify genes associated with polyQ expansion and subcellular localization of CTF, we analyzed gene expression profiles of PC12 rat pheochromocytoma cells using Tet-off system.

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Project description:Huntington’s disease is a monogenic disorder, with only one known causative gene, huntingtin (HTT). Expansion of a trinucleotide (CAG) repeat within the HTT gene results in a mutant protein containing polyglutamine (polyQ) stretches. While mutant HTT is the primary driver of cellular degeneration in the brain, the molecular and cellular mechanisms are incompletely understood. To further understand the role of polyQ in disease pathogenesis, we studied the dynamics of HTT protein-protein interactions (PPIs) in the striatum of mice with wild-type (Q20) and mutant (Q140) HTT at pre-symptomatic and manifest HD ages using label-free and isotope-labeled IP-MS approaches. Combining these approaches, we demonstrated that HTT PPI dynamics are distinct in early and later disease phases. Computational analysis pointed to early protein interaction changes involving synaptic transmission and vesicle fusion functions, while later interactions underlie changes in synapse morphogenesis and impact the actin cytoskeletal network.

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