SAM68-Specific Splicing Is Required for Proper Selection of Alternative 3' UTR Isoforms in the Nervous System

Iijima, Yoko and Tanaka, Masami and Suzuki, Satoko and Hauser, David and Tanaka, Masayuki and Okada, Chisa and Ito, Masatoshi and Ayukawa, Noriko and Sato, Yuji and Ohtsuka, Masato and Scheiffele, Peter and Iijima, Takatoshi. (2019) SAM68-Specific Splicing Is Required for Proper Selection of Alternative 3' UTR Isoforms in the Nervous System. iScience, 22. pp. 318-335.

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Official URL: https://edoc.unibas.ch/73873/

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Neuronal alternative splicing is a core mechanism for functional diversification. We previously found that STAR family proteins (SAM68, SLM1, SLM2) regulate spatiotemporal alternative splicing in the nervous system. However, the whole aspect of alternative splicing programs by STARs remains unclear. Here, we performed a transcriptomic analysis using SAM68 knockout and SAM68/SLM1 double-knockout midbrains. We revealed different alternative splicing activity between SAM68 and SLM1; SAM68 preferentially targets alternative 3' UTR exons. SAM68 knockout causes a long-to-short isoform switch of a number of neuronal targets through the alteration in alternative last exon (ALE) selection or alternative polyadenylation. The altered ALE usage of a novel target, interleukin 1 receptor accessory protein (Il1rap), results in remarkable conversion from a membrane-bound type to a secreted type in Sam68; KO; brains. Proper ALE selection is necessary for IL1RAP neuronal function. Thus the SAM68-specific splicing program provides a mechanism for neuronal selection of alternative 3' UTR isoforms.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Neurobiology > Cell Biology (Scheiffele)
UniBasel Contributors:Scheiffele, Peter
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Cell Press
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:23 Jun 2020 13:02
Deposited On:19 Jun 2020 13:55

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