Researchers have discovered a crucial link between an enzyme’s absence and brain function impairment. The study found that mice lacking the TRMT10A gene had significantly lower levels of tRNA, leading to impaired protein synthesis in the brain and compromised synapse structure. This deficiency resulted in diminished cognitive abilities and neuronal dysfunction.
The research, conducted at Kumamoto University, highlights the importance of a universal tRNA modification process in supporting brain function. By analyzing mice lacking the Trmt10a gene, the team identified a reduction in specific types of tRNAs essential for protein synthesis. This decrease led to decreased protein synthesis rates in key genes associated with neuronal function.
The study’s findings suggest that while tRNA levels were lower across various tissues, brain tissue was particularly affected. The researchers created mice lacking the Trmt10a gene and measured tRNA levels in their brains, discovering a significant decline in two types of tRNAs: initiator methionine tRNA and glutamine tRNA.
Consequently, protein synthesis rates decreased, leading to diminished cognitive abilities. Notably, while body weight was lower and hippocampal postsynaptic densities were smaller in the mice, no defects were observed in the pancreas, liver, or kidney.
The research team’s leader, Takeshi Chujo, stated that human cells lacking TRMT10A exhibited similar reductions in tRNA levels, suggesting that the mechanisms discovered in mice may also apply to humans. This study underscores the significance of tRNA modification during translation and paves the way for novel therapeutic approaches targeting intellectual disabilities caused by tRNA modification deficiencies.
The research sheds light on RNA modification diseases and offers innovative strategies for addressing cognitive challenges linked to these conditions.
Source: https://neurosciencenews.com/trna-synaptic-plasticity-27711/