From Hydra to rotifer and beyond: implications for human aging and delayed senescence (IMAGE)
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Figure 1. Detailed flowchart of the iterative experimental strategy to delay senescence by introducing Hydra-like gene expression in rotifers (Brachionus manjavacas). Key manipulations target rotifer orthologs (primarily FoxO and stemness markers) via CRISPR. Evaluation endpoints include lifespan/mortality hazard (survival curves), fertility (fecundity curves), locomotion (swimming assays), stress resistance, and transcriptomics (pre/post similarity to Hydra stem/progenitor states; ≥0.7 correlation threshold). Neoplasia monitoring uses proliferation markers (BrdU/phospho-histone H3) and deviation from Hydra tumor profiles. Iteration decisions are guided by predefined criteria (healthspan extension, transcriptomic shift, fitness constraints). Controls: wild-type and mock-treated rotifers. The framework also tests intercellular competition and multicellular aging through integrated measurements of cellular degradation, vigor-cooperation correlation, cheater emergence (neoplasia proxies), and negative senescence potential (mortality hazard). “Hydra-like” is defined in the text.
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Copyright: © 2026 Bordonaro et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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