Transposons comprise half of the our genome and are often dismissed as genomic ballast that threatens cellular integrity if not silenced (in part by piRNAs). However, our findings suggest that the interaction between transposons and their host cells is highly context-dependent and, in some cases, mutually beneficial. Consequently, the host silencing machinery does not apply a uniform block; instead, it appears to calibrate the vigor of its repression based on specific transposon families and individual copies. Using an integrated genomic, molecular, and computational framework, we dissect this intricate interplay to unravel how transposons actively shape cellular health.

During DNA replication, some degree of error is unavoidable. And genomic integrity is further challenged by endogenous radicals, external radiation, and the invasive activity of transposons, all of which can induce double-strand DNA breaks. To sustain their remarkable lifespan, planarian neoblasts must rigorously defend against and repair such damage. We use molecular and cell biological approaches to investigate the specific mechanisms these cells use to mitigate DNA damage and preserve their genomic stability over time.