How starving neurons form 'ribosome pairs' to survive food shortages

How starving neurons form 'ribosome pairs' to survive food shortages

Christina Sanchez
Christina Sanchez
2 Min.
A page from a book featuring a detailed illustration of a plant cell, including labeled parts such as the nucleus and mitochondria, with accompanying text describing the cell's structure and function.

How starving neurons form 'ribosome pairs' to survive food shortages

Scientists have uncovered how neurons save energy during food shortages by forming inactive pairs of ribosomes, called disomes. These structures are created when RNA 'tentacles' link ribosomes together under stress, offering new insights into animal cell survival mechanisms.

Researchers at the Max Planck Institute for Brain Research used cryo-electron tomography to observe disomes in frozen cells for the first time. The technique revealed that expansion segment 31b—a flexible RNA strand—forms a 'kissing loop' to bind two ribosomes into a stable, reversible pair.

The study combined cell biology, biochemistry, and genetic experiments in yeast and mammalian cells. Unlike bacteria, animal cells rely on these long RNA structures to connect ribosomes when nutrients are scarce. By storing ribosomes as inactive pairs, cells protect them from damage and allow quick reactivation once conditions improve.

This discovery builds on earlier work, including a 2021 Nature paper by Juszkiewicz et al., which explored ZNF598-mediated disome surveillance in mammals. Recent studies, such as a 2024 Cell investigation into hepatic steatosis and NIH-funded research on ALS, have linked disomes to stress management in diseases like neurodegeneration and cancer. These inactive ribosome pairs trigger stress granules and inflammation in organs such as the brain and liver.

The findings provide a clearer picture of how animal cells manage stress and maintain ribosome function. Understanding disome formation could lead to new research into their role in health and disease, particularly in conditions tied to translational stress. Scientists now have a foundation for exploring how ribosome organisation affects recovery from cellular damage.

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