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A pioneering study undertaken by a Kumamoto University research team shed light on the crucial role of TRMT10A, a tRNA methylation enzyme, in sustaining brain function. The findings show how TRMT10A deficiency reduces specific transfer RNA (tRNA) levels in the brain, altering protein synthesis and affecting synapse structure and function.
The researchers generated mice deficient in the Trmt10a gene and assessed tRNA levels in the brain. They found a large drop in two types of tRNA: the initiator methionine tRNA, which is required for protein synthesis, and a particular glutamine tRNA. This reduction resulted in less protein production of essential genes in the brain, notably those involved in neuronal function. Consequently, the structural integrity and flexibility of synapses--crucial. Remarkably, while a decrease in initiator methionine and glutamine tRNA levels was observed throughout various tissues, functional impairments were limited to the brain, indicating its particular vulnerability. Lecturer Takeshi Chujo from the Faculty of Life Sciences, Kumamoto University, who led the research, stated: "Since human cells lacking TRMT10A exhibited similar reductions in these tRNA levels, it suggests that the mechanisms we discovered in mice could likely apply to humans as well." The study highlights the importance of a universal tRNA modification for translation of specific codons. With these insights, the research team aims to explore whether preventing the decline of tRNA levels in the brain could mitigate functional impairments, potentially leading to novel therapeutic approaches for treating intellectual disabilities caused by tRNA modification deficiencies. This research not only enhances our understanding of RNA modification diseases but also opens doors to innovative strategies for addressing cognitive challenges linked to these conditions. (ANI)
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