Across three Drosophila species, older males showed more upregulated transposable element copies than females, yet this increase did not correspond to shorter lifespan. Swapping Y chromosomes between strains altered male longevity in a strain-specific manner despite comparable Y chromosome size, pointing to heterochromatic variation and gene interactions rather than overall repetitive element burden. The findings constrain the "toxic Y" explanation for why females outlive males.
Key Points
- Older males upregulated more transposable element copies than females consistently
- Elevated element expression did not predict shortened male lifespan
- Y chromosome swaps changed male longevity independent of chromosome size
Longevity Analysis
Sex differences in lifespan are frequently attributed to a single mechanism, and this work narrows one of the leading candidates: the age-related loosening of epigenetic silencing over repetitive DNA may be a marker of genomic aging rather than its driver. Accurate attribution matters, because interventions aimed at restoring heterochromatin stability are being pursued as regenerative strategies, and the target must be correctly identified before effort is directed at it. The results favor interactions between chromosomal regions over raw element abundance, a reminder that aging signals read in isolation are easily misassigned.
Original published by Wiley Aging Cell, by Miriam Merenciano, Sonia Janillon, Camille Mermet‐Bouvier, Nelly Burlet, Valentina Rodriguez‐Rada, Victor Ronget, Patricia Gibert, Jean‐Michel Gaillard, Jean‐François Lemaitre, Gabriel A. B. Marais, Matthieu Boulesteix, Marie Fablet, Cristina Vieira.