Mechanism for Coping with Ribosomes Stalled on mRNAs with Premature Stop Codons

New research from the Case Western Reserve University School of Medicine describes a mechanism by which an essential quality control system in cells identifies and destroys faulty genetic material. The findings were published online on December 23, 2016 in Nature Communications. The open-access article is titled ATP Hydrolysis by UPF1 Is Required for Efficient Translation Termination at Premature Stop Codons.” Kristian Baker Ph.D., Associate Professor in the Center for RNA Molecular Biology at Case Western Reserve University School of Medicine, led the study that provided evidence for direct communication between the cell's protein synthesis machinery - the ribosome - and the protein complex that recognizes and destroys defective genetic intermediates called messenger RNAs (mRNAs). "We aimed to understand how cells are able to recognize mRNA that is defective and distinguish it from normal mRNA. For most cells, this process is critical for survival, but we didn't yet understand how it works, especially when the difference between the two is very subtle," said Dr. Baker. "Our findings clearly show that surveillance machinery involved in identifying faulty mRNA functionally interacts with the ribosome, the apparatus responsible for synthesizing proteins in the cell. It is now clear that these two elements communicate and work closely together to recognize and eliminate aberrant mRNA from the cell." Cells convert sections of DNA encoding genes into mRNA that serves as a blueprint for the synthesis of a protein.
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