Abstract
Longevity is influenced by genetic and environmental factors, but the underlying mechanisms remain elusive. Here, we functionally characterise a Drosophila small nucleolar RNA (snoRNA), named jouvence whose loss of function reduces lifespan. The genomic region of jouvence rescues the longevity in mutant, while its overexpression in wild-type increases lifespan. Jouvence is required in enterocytes. In mutant, the epithelium of the gut presents more hyperplasia, while the overexpression of jouvence prevents it. Molecularly, the mutant lack pseudouridylation on 18S and 28S-rRNA, a function rescued by targeted expression of jouvence in the gut. A transcriptomic analysis performed from the gut reveals that several genes are either up- or down-regulated, while restoring the mRNA level of two genes (ninaD or CG6296) rescue the longevity. Since snoRNAs are structurally and functionally well conserved throughout evolution, we identified putative jouvence orthologue in mammals including humans, suggesting that its function in longevity could be conserved.
Highlights
Longevity is influenced by genetic and environmental factors, but the underlying mechanisms remain elusive
In a study to characterize putative genes involved in locomotor activity and more genes expressed in the central complex (CC), a premotor centre localised in the middle of the brain[31], a P-element insertional mutagenesis was performed
Both genes were normally expressed in the deletion line compared to control Wild-Type (WT) Canton-S (CS) flies (Supplementary Fig. 1b)
Summary
Longevity is influenced by genetic and environmental factors, but the underlying mechanisms remain elusive. We functionally characterise a Drosophila small nucleolar RNA (snoRNA), named jouvence whose loss of function reduces lifespan. The genomic region of jouvence rescues the longevity in mutant, while its overexpression in wild-type increases lifespan. 1234567890():,; The aging process is the result of complex biological mechanisms leading to accumulation of different types of damage at molecular, cellular, tissue and organ levels This leads to the decrease or loss of certain physiological functions, and to an increase of vulnerability to diseases and death[1,2]. As snoRNAs are generally well conserved throughout evolution, both structurally and functionally, we identify putative jou mammalian orthologues, both in mouse and human, suggesting that it may have an implication in mammalian aging
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