Key result
The GM-CSF AU-rich element repressed translation independently of its effect on mRNA levels, likely by interfering with poly(A)-binding protein-mediated mRNA circularization.
The GM-CSF AU-rich element controls translation and mRNA decay by interfering with poly(A)-binding protein-mediated mRNA circularization.
Animal data suggest AU-rich element control of inflammatory mediators; leaves open relevance to human cardiovascular disease.
The AU-rich element (ARE) controls the turnover of many unstable mRNAs and their translation. The granulocyte-macrophage colony-stimulating factor (GM-CSF) ARE is known to be a destabilizing element, but its role in translation remains unclear. Here we studied in vivo the role of the GM-CSF ARE on the mRNA and protein expressions of an enhanced green fluorescent protein reporter gene. The GM-CSF ARE had a repressor effect on translation independently of its effect on mRNA levels. In the context of an internal ribosome entry site, the GM-CSF ARE still repressed translation but was no longer functional as a destabilizing element. Gel retardation assays showed that poly(A)-binding protein is displaced from the poly(A) tail when the ARE is present in the 3'-untranslated region. These data suggest that the GM-CSF ARE controls translation and mRNA decay by interfering with poly(A)-binding protein-mediated mRNA circularization.
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Grosset et al. (2004) studied this question. GM-CSF AU-rich element (ARE) was evaluated on mRNA and protein expressions of an enhanced green fluorescent protein reporter gene. The GM-CSF AU-rich element repressed translation independently of its effect on mRNA levels, likely by interfering with poly(A)-binding protein-mediated mRNA circularization.
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