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Translational attenuation mediated by an mRNA intron
1Howard Hughes Medical Institute, Department of Biochemistry and Biophysics, University of California School of Medicine, San Francisco 94143-0448, USA.
Current Biology : CB
|February 28, 1998
Summary
The HAC1 mRNA intron prevents translation, even when the mRNA is in the cytoplasm. This finding reveals a novel mechanism for regulating gene expression via mRNA introns.
Area of Science:
- Molecular Biology
- Cell Biology
- Gene Expression Regulation
Background:
- The unfolded protein response (UPR) is activated by endoplasmic reticulum (ER) stress.
- UPR activation involves regulated splicing of HAC1 mRNA to produce the Hac1p transcription factor.
- Uninduced HAC1 mRNA (HAC1u) is stable but does not produce detectable Hac1p.
Purpose of the Study:
- To investigate why unspliced HAC1 mRNA (HAC1u) does not produce Hac1p.
- To determine the role of the HAC1 intron in translation regulation.
Main Methods:
- Tracking HAC1u mRNA localization and polyribosome association.
- Assessing Hac1p production from unspliced and spliced HAC1 mRNA.
- Analyzing Hac1p modification and activity.
- Transplanting the HAC1 intron into a heterologous mRNA system.
Main Results:
- HAC1u mRNA is exported to the cytosol and associates with polyribosomes.
- The HAC1 intron prevents translation of HAC1u mRNA.
- Hac1p produced from unspliced mRNA (Hac1pu) is less active than Hac1pi.
- The HAC1 intron alone can attenuate translation of other mRNAs.
Conclusions:
- The HAC1 mRNA intron is essential and sufficient to block translation of polyribosome-associated mRNA.
- This study identifies a novel mechanism of translational attenuation mediated by an mRNA intron.