BREs Mediate Both Repression and Activation of oskar mRNA Translation and Act In trans

Asymmetric positioning of proteins within cells is crucial for cell polarization and function. Deployment of Oskar protein at the posterior pole of the Drosophila oocyte relies on localization of the oskar mRNA, repression of its translation prior to localization, and finally activation of translati...

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Published inDevelopmental cell Vol. 18; no. 3; pp. 496 - 502
Main Authors Reveal, Brad, Yan, Nan, Snee, Mark J., Pai, Chin-I., Gim, Youme, Macdonald, Paul M.
Format Journal Article
LanguageEnglish
Published Cambridge, MA Elsevier Inc 16.03.2010
Cell Press
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Summary:Asymmetric positioning of proteins within cells is crucial for cell polarization and function. Deployment of Oskar protein at the posterior pole of the Drosophila oocyte relies on localization of the oskar mRNA, repression of its translation prior to localization, and finally activation of translation. Translational repression is mediated by BREs, regulatory elements positioned in two clusters near both ends of the oskar mRNA 3′ UTR. Here we show that some BREs are bifunctional: both clusters of BREs contribute to translational repression, and the 3′ cluster has an additional role in release from BRE-dependent repression. Remarkably, both BRE functions can be provided in trans by an oskar mRNA with wild-type BREs that is itself unable to encode Oskar protein. Regulation in trans is likely enabled by assembly of oskar transcripts in cytoplasmic RNPs. Concentration of transcripts in such RNPs is common, and trans regulation of mRNAs may therefore be widespread. ► Before localization, oskar mRNA translation repressed via BREs in the 3′ UTR ► Some BREs also are bifunctional and also mediate translational activation ► Both BRE functions can act in trans between different oskar transcripts ► Cytoplasmic RNP assembly may facilitate trans activity of regulatory elements
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Present address: Department of Genetics, Washington University in St. Louis, St. Louis, MO 63110, USA
Present address: Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA
ISSN:1534-5807
1878-1551
DOI:10.1016/j.devcel.2009.12.021