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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.

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