A Long Noncoding RNA on the Ribosome Is Required for Lifespan Extension
Paul B. Essers,
Julie Nonnekens,
Yvonne J. Goos,
Marco C. Betist,
Marjon D. Viester,
Britt Mossink,
Nico Lansu,
Hendrik C. Korswagen,
Rob Jelier,
Arjan B. Brenkman,
Alyson W. MacInnes
Affiliations
Paul B. Essers
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Julie Nonnekens
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Yvonne J. Goos
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Marco C. Betist
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Marjon D. Viester
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Britt Mossink
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Nico Lansu
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Hendrik C. Korswagen
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
Rob Jelier
Centre of Microbial and Plant Genetics, KU Leuven, Kasteelpark Arenberg 20, 3001 Leuven, Belgium
Arjan B. Brenkman
Section Metabolic Diseases, Department of Molecular Cancer Research, Wilhelmina Children’s Hospital, University Medical Center Utrecht, 3508 AB Utrecht, the Netherlands
Alyson W. MacInnes
Hubrecht Institute, KNAW and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands
The biogenesis of ribosomes and their coordination of protein translation consume an enormous amount of cellular energy. As such, it has been established that the inhibition of either process can extend eukaryotic lifespan. Here, we used next-generation sequencing to compare ribosome-associated RNAs from normal strains of Caenorhabditis elegans to those carrying the life-extending daf-2 mutation. We found a long noncoding RNA (lncRNA), transcribed telomeric sequence 1 (tts-1), on ribosomes of the daf-2 mutant. Depleting tts-1 in daf-2 mutants increases ribosome levels and significantly shortens their extended lifespan. We find tts-1 is also required for the longer lifespan of the mitochondrial clk-1 mutants but not the feeding-defective eat-2 mutants. In line with this, the clk-1 mutants express more tts-1 and fewer ribosomes than the eat-2 mutants. Our results suggest that the expression of tts-1 functions in different longevity pathways to reduce ribosome levels in a way that promotes life extension.