(Submitter supplied) As a newly evolved duplicated gene of TARS1 (encoding cytoplasmic threonyl-tRNA synthetase), TARSL2 (TARS3) encodes a protein highly similar with TARS1 with only obvious difference in N-terminus. Albeit with tRNA charging activity in vitro and incorporated into the multiple tRNA synthetase complex (MSC), whether TARSL2 is able to function as a tRNA synthetase to substitute TARS1 in vivo is unclear. In this work, we found that Tars1 was essential for embryonic development. In contrast, knockout of Tarsl2 was achievable. Loss of Tarsl2 had no effect on both abundance and charging levels of all tRNAThr isoacceptors, indicating Tarsl2 is not for tRNAThr metabolism. Furthermore, Tarsl2 deletion did not influence protein levels of other MSC components, MSC integrity and aminoacylation levels of non-cognate tRNAs by MSC components. However, a severe retardation of mice development was observed after 3 weeks accompanied with an elevated metabolism capacity and muscle development abnormity. We further constructed a Tarsl2-deleted zebrafish, which exhibited no change in the level and charging of tRNAThrs. Collectively, these data suggest that Tarsl2 is evolved not for canonical tRNAThr aminoacylation and cannot substitute Tars1 in vivo.
- Organism:
- Mus musculus
- Type:
- Expression profiling by high throughput sequencing
- Platform:
- GPL13112
- 6 Samples
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