ECP Knockdown Extends Life in Flies, Probably via AMPK
Permalink | View Comments (0) | Post Comment | | Posted by Reason

Too many ways to modestly slow aging in lower animals are being discovered nowadays to mention them all. These methods generally involve altering levels of one or more proteins, and then observing the resulting effects on metabolism and life span. As knowledge of the various pathways and mechanisms involved expands, it is becoming clear that most interventions discovered over the past two decades are linked to one another, being just different points of influence in the same larger set of mechanisms. So it isn't unusual at all for a novel method of life extension in laboratory animals to be connected to other, previously discovered methods, and that is the case here:

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.

Eukaryotic initiation factor 5 C-terminal domain containing protein (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.

Link: http://dx.doi.org/10.1016/j.bbrc.2014.02.133

Comments
Post a comment; thoughtful, considered opinions are valued. Please note that comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.









Remember personal info?