ELAV mediates 3' UTR extension in the Drosophila nervous system

Hilgers, Valérie; Lemke, Sandra B.; Levine, Michael

doi:10.1101/gad.199653.112

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ELAV mediates 3' UTR extension in the Drosophila nervous system

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Hilgers, Valérie
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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http://genesdev.cshlp.org/content/26/20/2259.long
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Citation

Hilgers, V., Lemke, S. B., & Levine, M. (2012). ELAV mediates 3' UTR extension in the Drosophila nervous system. Proceedings of the National Academy of Sciences of the United States of America, 26, 2259-2264. doi:10.1101/gad.199653.112.

Cite as: https://hdl.handle.net/21.11116/0000-0006-0444-9

Abstract

Post-transcriptional gene regulation is prevalent in the nervous system, where multiple tiers of regulatory complexity contributeto the development and function of highly specialized cell types. Whole-genome studies in Drosophila have identified several hundred genes containing long 3′ extensions in neural tissues. We show that ELAV (embryonic-lethalabnormal visual system) is a key mediator of these neural-specific extensions. Misexpression of ELAV results in the ectopicsynthesis of long messenger RNAs (mRNAs) in transgenic embryos. RNA immunoprecipitation assays suggest that ELAV directlybinds the proximal polyadenylation signals of many target mRNAs. Finally, ELAV is sufficient to suppress 3′ end formationat a strong polyadenylation signal when tethered to a synthetic RNA. We propose that this mechanism for coordinating 3′ UTRextension may be generally used in a variety of cellular processes.