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RESEARCH PAPER

Sex-lethal imparts a sex-specific function to UNR by recruiting it to the msl-2 mRNA 3' UTR: translational repression for dosage compensation

¹ Gene Expression Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany; ² Centre de Regulació Genómica (CRG-UPF), 08003 Barcelona, Spain

MSL-2 (male-specific lethal 2) is the limiting component of the Drosophila dosage compensation complex (DCC) that specifically increases transcription from the male X chromosome. Ectopic expression of MSL-2 protein in females causes DCC assembly on both X chromosomes and lethality. Inhibition of MSL-2 synthesis requires the female-specific protein sex-lethal (SXL), which binds to the msl-2 mRNA 5' and 3' untranslated regions (UTRs) and blocks translation through distinct UTR-specific mechanisms. Here, we purify translationally silenced msl-2 mRNPs and identify UNR (upstream of N-ras) as a protein recruited to the 3' UTR by SXL. We demonstrate that SXL requires UNR as a corepressor for 3'-UTR-mediated regulation, imparting a female-specific function to the ubiquitously expressed UNR protein. Our results reveal a novel functional role for UNR as a translational repressor and indicate that UNR is a key component of a "fail-safe" dosage compensation regulatory system that prevents toxic MSL-2 synthesis in female cells.

[Keywords: Translational control; dosage compensation; mRNP; cold shock domain; female cell line; sex-specific function]

Received October 27, 2005; revised version accepted December 1, 2005.

Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.371406.

³ Present address: Program in Developmental and Stem Cell Biology, University of California, San Francisco, CA 94143, USA.

⁴ Corresponding author.

E-MAIL hentze{at}embl.de; FAX 49-6221-387518.

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