Abstract：
:Most aging hypotheses assume the accumulation of damage, resulting in gradual physiological decline and, ultimately, death. Avoiding protein damage accumulation by enhanced turnover should slow down the aging process and extend the lifespan. However, lowering translational efficiency extends rather than shortens the lifespan in C. elegans. We studied turnover of individual proteins in the long-lived daf-2 mutant by combining SILeNCe (stable isotope labeling by nitrogen in Caenorhabditiselegans) and mass spectrometry. Intriguingly, the majority of proteins displayed prolonged half-lives in daf-2, whereas others remained unchanged, signifying that longevity is not supported by high protein turnover. This slowdown was most prominent for translation-related and mitochondrial proteins. In contrast, the high turnover of lysosomal hydrolases and very low turnover of cytoskeletal proteins remained largely unchanged. The slowdown of protein dynamics and decreased abundance of the translational machinery may point to the importance of anabolic attenuation in lifespan extension, as suggested by the hyperfunction theory.
journal_name
Cell Repjournal_title
Cell reportsauthors
Dhondt I,Petyuk VA,Cai H,Vandemeulebroucke L,Vierstraete A,Smith RD,Depuydt G,Braeckman BPdoi
10.1016/j.celrep.2016.07.088subject
Has Abstractpub_date
2016-09-13 00:00:00pages
3028-3040issue
11issn
2211-1247pii
S2211-1247(16)31069-5journal_volume
16pub_type
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