Study unveils novel crosstalk mechanism between mitochondrial translation and cytoplasmic translation

Credit: Image by QIN Yan's Group

Source: Chinese Academy of Sciences Headquarters | Summary: By using a systemic mtEF4 gene knockout mouse model, researchers have found that mtEF4 knockout damages the oxidative phosphorylation function in germ cells of male mice, thus causing male sterility.

"Protein is the fundamental substance of life. The genetic code directing protein synthesis is stored in DNA. When a cell is instructed, the code information transfers from DNA to mRNA. Then, information on mRNA is further transferred to protein.

There are two sets of protein translation systems in mammalian cells -- the cytoplasmic translation system and the mitochondrial translation system -- both of which are composed of ribosome, tRNAs and translation factors. The translation system translates mRNA into biologically competent protein according to the information on mRNA. However, the coordination mechanism between the cytoplasmic translation system and the mitochondrial translation system has been a mystery.

A research article entitled "Mammalian Elongation Factor 4 Regulates Mitochondrial Translation Essential for Spermatogenesis" was published online in the journal Nature Structural & Molecular Biology on April 11, 2016. It describes the crosstalk mechanism between mitochondrial translation and cytoplasmic translation..."

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https://www.sciencedaily.com/releases/2016/04/160414095410.htm