Knockdown expression of eukaryotic initiation factor 5 C-terminal domain containing protein extends lifespan in Drosophila melanogaster

•Knockdown of ECP results in extended lifespan and better locomotor performance.•AMPK was activated when ECP was inhibited.•Inhibition of ECP leads to reduced AKT and S6K activity.•Inhibition of ECP leads to enhancement of mitochondria function. Inhibition of translation by mutations of a growing number of genes involved in protein synthesis could extend healthy lifespan in yeast, worm, fly and mouse as well. These genes vary from translation initiation factors to structural components of ribosomes and ribosomal RNA processing factors. ECP is a novel ribosome associated protein. Previous data supports the involvement of this gene in long term memory formation and exon guidance in Drosophila probably through its still unconfirmed functions in protein synthesis. However, the exact molecular function of ECP is still largely unknown. Our findings here show that fly lifespan could be significantly extended in ECP RNAi flies. Meanwhile, the locomotion ability of elder ECP RNAi flies was also improved remarkably. Further studies revealed an increase of mitochondria Complex IV activity in these ECP RNAi flies. A decrease of AKT and S6K phosphorylation level in contrast to an increase of AMPK phosphorylation level could also be detected in these flies. Together, these findings support a positive effect of ECP on longevity and delaying age-related impairment in locomotor behavior probably through activation of AMPK and enhancement of mitochondrial function via insulin/IGF-1 and TOR pathway.