Kumamoto University Uncovers Critical Role of TRMT10A in Brain Function

A study by Kumamoto University has identified TRMT10A as crucial for sustaining brain function. The research reveals TRMT10A deficiency impacts tRNA levels, altering protein synthesis and synapse structure, specifically in the brain. The findings could pave the way for new treatments for intellectual disabilities.

A groundbreaking study from Kumamoto University has delineated the critical function of TRMT10A, an enzyme responsible for tRNA methylation, in maintaining brain health. Researchers demonstrated that a deficiency in TRMT10A leads to a significant reduction in specific transfer RNA (tRNA) levels within the brain, consequently altering protein synthesis and impacting synapse structure and functionality.

In their experiments, the team engineered mice lacking the Trmt10a gene and analyzed tRNA levels, discovering a substantial reduction in two types of tRNA: the initiator methionine tRNA, necessary for protein synthesis, and a particular glutamine tRNA. This reduction correlated with decreased production of essential proteins required for neuronal function, thereby compromising the synaptic integrity and flexibility.

Interestingly, although similar tRNA reductions were noted across different tissues, the functional impairments were restricted to the brain, highlighting its unique susceptibility. Lecturer Takeshi Chujo from Kumamoto University noted that human cells devoid of TRMT10A exhibited comparable tRNA reductions, suggesting that these mechanisms might also be applicable to humans. The research underscores the importance of universal tRNA modification in protein translation and opens potential avenues for developing therapies targeting intellectual disabilities associated with tRNA modification deficits.

(With inputs from agencies.)