This is a fascinating and elegant study that elucidates a key mechanism controlling the translation (or halt thereof) of proteins whose mRNAs lack a stop codon. The core findings of the paper are nicely summarized on the site. The potentially exciting thing about this mechanism is a novel explanation for a rather fundamental issue in protein quality control, and a potential piece of the puzzle in "proteostasis" in neurodegenerative disorders. The mechanistic conservation of listern in mammals and Ltn1 in yeast is of interest.
From a disease biology perspective, it will be important to determine whether listerin/Ltn1 mechanisms are impaired or lost with the large variety of age-related neurodegenerations. Alternatively, perhaps augmentation of listerin/Ltn1 could be exploited to improve protein synthetic quality control during periods of stress or aging.
Comments
This is a fascinating and elegant study that elucidates a key mechanism controlling the translation (or halt thereof) of proteins whose mRNAs lack a stop codon. The core findings of the paper are nicely summarized on the site. The potentially exciting thing about this mechanism is a novel explanation for a rather fundamental issue in protein quality control, and a potential piece of the puzzle in "proteostasis" in neurodegenerative disorders. The mechanistic conservation of listern in mammals and Ltn1 in yeast is of interest.
From a disease biology perspective, it will be important to determine whether listerin/Ltn1 mechanisms are impaired or lost with the large variety of age-related neurodegenerations. Alternatively, perhaps augmentation of listerin/Ltn1 could be exploited to improve protein synthetic quality control during periods of stress or aging.
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