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Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
Published on: October 28, 2014
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Hrp48 and eIF3d contribute to msl-2 mRNA translational repression
Emilia Szostak1,2, Marina García-Beyaert1,2, Tanit Guitart1,2
1Gene Regulation, Stem Cells and Cancer Programme, Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain.
Nucleic Acids Research
|April 11, 2018
Summary
Sex-lethal (SXL) uses Hrp48 to repress msl-2 mRNA translation in female Drosophila. Hrp48 targets translation initiation factor eIF3d, revealing a mechanism for mRNA-specific translational control.
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- Translational repression of msl-2 mRNA is crucial for dosage compensation in female Drosophila melanogaster.
- Sex-lethal (SXL) protein regulates this repression by binding to msl-2 untranslated regions (UTRs), but the precise mechanism remains unclear.
Purpose of the Study:
- To identify co-factors involved in SXL-mediated translational repression of msl-2 mRNA.
- To elucidate the molecular mechanisms by which SXL inhibits translation initiation.
Main Methods:
- RNA immunoprecipitation and reporter assays were used to identify and characterize SXL co-factors.
- RNA chromatography and depletion studies were employed to investigate the role of translation initiation factors.
Main Results:
- Hrp48 was identified as a Sex-lethal (SXL) co-factor that binds the msl-2 3' UTR and is essential for repression.
- Hrp48 interacts with eIF3d, a subunit of the eIF3 translation initiation complex.
- eIF3d binds the msl-2 5' UTR and is required for both translation and repression; its depletion de-represses msl-2 expression.
Conclusions:
- Hrp48 inhibits msl-2 translation by targeting the translation initiation factor eIF3d.
- This study reveals a novel mechanism for mRNA-specific translational control, where general translation factors are co-opted by RNA-binding proteins.
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