Russian researchers identify a cellular mechanism that links energy production to learning
Scientists have pinpointed a cellular mechanism whose disruption makes learning harder, a discovery reported in a leading scientific journal. The finding underscores a vital connection between how energy is produced in cells and cognitive function. In the cell, mitochondria act as power plants, supplying the energy necessary for countless biological processes. They also participate in one of the two distinct pathways by which genetic information becomes functional proteins. Although mitochondria are known to host ribosomes, the tiny protein factories inside the organelle, the precise steps of how these ribosomes are assembled remain only partially understood. This gap has left a missing piece in the broader picture of how energy supply and protein synthesis coordinate within this essential cellular compartment.
Two years prior, researchers identified two enzymes that modify ribosomal RNA and contribute directly to mitochondrial ribosome assembly. By examining the intermediate stages of this assembly, the team mapped exactly where these enzymes—ribosomal methyltransferases—work, how they support construction, and where the process can fail. Moscow-based scientist Petr Sergiev, head of the State University Institute of Functional Genomics and a corresponding member of the Russian Academy of Sciences, described this work as a major step toward understanding mitochondrial biology. The evidence suggests that these enzymes play a central role in guiding the maturation of ribosomes inside mitochondria, and that proper ribosome assembly is essential for cellular energy management and downstream cellular activities.
In a series of functional experiments, the team engineered cells that no longer produced the enzymes required for mitochondrial ribosome assembly. They extended this approach to animal models by producing mice with inactivated versions of the same enzymes. The physiological effects were striking and instructive: the animals showed reduced vitality, diminished resilience, and notable impairment in tasks related to learning. In a common behavioral test, a mouse is placed in an arena with multiple exits and must identify the correct route to escape. While ordinary mice quickly learn and choose the correct exit on subsequent trials, the enzyme-inactivated mice repeatedly search for the exit, unable to form or recall an efficient escape strategy. This pattern demonstrates how disruptions in mitochondrial function can translate into observable deficits in learning and behavior.
The researchers connect these behavioral changes to energy management at the cellular level. Mitochondria supply the energy that powers muscle movement and cognitive processing. When mitochondrial function is compromised, the most energy-demanding activities—muscle contraction and higher-order thinking—are among the first to suffer. The study therefore points to a direct link between mitochondrial ribosome assembly, energy production, and the brain’s capacity to learn. The authors emphasize that the integrity of ribosomal RNA modification and ribosome assembly in mitochondria is crucial for maintaining the energy balance required for learning-related neural processes. These findings add to a broader understanding of how energy metabolism intersects with memory formation and learning at the cellular level. The implications may extend to human health, offering potential insights into conditions where mitochondrial dysfunction and cognitive impairment co-occur. This work is discussed in the scientific literature and is cited in recent reviews of mitochondrial gene expression and its impact on neural function. (Citation: Nature, 2023.)