Qtrt1, queuine tRNA-ribosyltransferase 1, is a key component of the QTRT1-QTRT2 enzyme complex in mammals. It facilitates queuosinylation, a process introducing the modified nucleoside queuosine (Q) into specific tRNAs at the wobble position. This modification is crucial for ensuring translation fidelity and efficiency, and is involved in various biological processes [1,2,3,4,5,6].

Qtrt1 knockout mouse models have been instrumental in revealing its functions. Loss of Q-tRNA due to Qtrt1 knockout leads to learning and memory deficits, with female mice more severely affected. Ribo-Seq analysis in these mice showed ribosome stalling on Q-decoded codons and a global imbalance in translation elongation speed [1]. In breast cancer models, Qtrt1 deficiency in human breast cancer cells altered the functions of genes related to cell proliferation, tight junction formation, and migration both in vitro and in vivo, and also changed the abundance of certain core bacteria in tumors [4]. In inflammatory bowel disease, Qtrt1 expression was significantly downregulated in patients, and Qtrt1 knockout mice confirmed its role in cell proliferation, intestinal junctions, and inflammation [2].

In conclusion, Qtrt1 plays essential roles in maintaining translation-related processes and is involved in various disease conditions. Studies using Qtrt1 knockout mouse models have provided valuable insights into its functions in learning and memory, breast cancer development, and inflammatory bowel disease, highlighting its potential as a therapeutic target in these disease areas.