Cancelled: Seminar "Elucidation of the physiological function of Ataxin-2, a neurodegeneration-associated RNA binding protein"

Date

Thursday, July 31, 2014 - 16:30 to 17:30

Location

C016, Lab1

Description

Speaker: Prof. Yukio Kawahara, Professor, Department of RNA Biology and Neuroscience, Graduate School of Medicine, Osaka University

Title: Elucidation of the physiological function of Ataxin-2, a neurodegeneration-associated RNA binding protein

Abstract: Spinocerebellar ataxia type 2 is an autosomal dominant neurodegenerative disease. The disorder is caused by abnormal CAG repeat expansion in the coding region of the Ataxin-2 gene (ATXN2). Recently, moderate CAG repeat expansion in ATXN2 was identified as a risk factor for amyotrophic lateral sclerosis. This finding suggests a common pathogenic role of Ataxin-2 in these neurodegenerative diseases. Therefore, a comprehensive understanding of the physiological functions of Ataxin-2 is necessary to elucidate the mechanism underlying Ataxin-2-mediated neurodegeneration. Ataxin-2 is known to directly bind to polyadenylate-binding protein 1 (PABPC1), which suggests that Ataxin-2 is likely involved in RNA metabolism. However, the functions of Ataxin-2 have not been characterized in detail. We have recently found that Ataxin-2 binds directly to some class of RNAs in a PABPC1-independent manner. High-throughput sequencing of Ataxin-2-bound RNAs revealed that Ataxin-2 binds predominantly to distinct elements in the 3’UTRs of target mRNAs. Gene expression analysis after Ataxin-2 depletion or overexpression revealed that Ataxin-2 stabilizes target mRNAs and increases the abundance of corresponding proteins. In this seminar, I would like to introduce how to identify targets and functions of Ataxin-2 in more detail and how disease-associated polyglutamine expansion affects the physiological activity of Ataxin-2.

Host: Tadashi Yamamoto, Cell Signal Unit

Sponsor or Contact: 
Kaori Yamashiro, Cell Signal Unit (Yamamoto Unit)
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