On the 30th, the reporter learned from Zhejiang University that in a study led by Professor Guan Minxin and Chen Yu, a professor at the Institute of Genetics of Zhejiang University, the team researchers used the gene editing technology to obtain the defect of the mitochondrial tRNA post-transcriptional modification gene mtu1 for the first time. The zebrafish model clarifies the molecular pathogenesis of the "culprit" mtu1 of deafness with a comprehensive research perspective. The research results were published online in the internationally authoritative academic journal "Nucleic Acid Research".
In this study, the team of Guan Minxin team first constructed the zebrafish model of mtu1 knockout, and explored the pathogenesis mechanism from multiple levels to determine the pathogenic mechanism of mtu1 leading to hereditary deafness, which is the energy required for hearing. The destruction of the power plant. When the mtu1 gene is mutated, there are three kinds of tRNAs that cannot accurately synthesize the protein "machine" of mitochondria-producing energy. The "machine" function is impaired and the power supply of the mitochondria "power plant" is insufficient. Inner ear hair cells are the most important thing in the perception of sound in living organisms. As a highly energy-consuming cell, it needs a large amount of mitochondria to supply energy during life-sustaining activities and functions. When the mtu1 gene affects mitochondrial function, this "power shortage" causes the auditory dysfunction of the organism.
This study provides a new scientific basis and treatment for the prevention and treatment of hereditary deafness. (Reporter Jiang Wei correspondent Ke Yieneng)
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