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Updated: May 24, 2026
09:13
In vivo Interrogation of Central Nervous System Translatome by Polyribosome Fractionation
Published on: April 30, 2014
Coding region polyadenylation generates a truncated tRNA synthetase that counters translation repression
Peng Yao1, Alka A Potdar, Abul Arif
1Department of Cell Biology, The Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Cell
|March 6, 2012
Summary
Researchers discovered a new mechanism controlling protein synthesis, where a truncated enzyme (EPRS(N1)) regulates gene expression by preventing translation inhibition. This finding reveals a novel way cells fine-tune protein production.
Area of Science:
- Molecular Biology
- Gene Regulation
- Posttranscriptional Control
Background:
- Gene transcription provides
- on-off
- switches for gene expression.
- Posttranscriptional mechanisms offer finer control over protein synthesis.
Purpose of the Study:
- To investigate the link between mRNA levels and protein synthesis.
- To elucidate the mechanism behind the gamma-interferon-activated inhibitor of translation (GAIT) complex's regulation of VEGF-A synthesis.
Main Methods:
- Computational modeling and experimental validation were used.
- Identification of GAIT complex components and their interactions.
- Analysis of mRNA and protein expression levels.
Main Results:
- The GAIT complex maintains a low, constant rate of VEGF-A synthesis, irrespective of mRNA levels.
- A truncated form of glutamyl-prolyl tRNA synthetase (EPRS(N1)) was identified as a factor interacting with GAIT elements.
- EPRS(N1) inhibits the GAIT complex, allowing a basal level of translation for target proteins.
Conclusions:
- The PAY(∗) mechanism generates truncated proteins like EPRS(N1) that regulate translation.
- This mechanism allows for a "translational trickle" of specific proteins.
- Genome-wide analysis suggests this is a general mechanism for producing regulatory proteins.
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