A. V. Annapragada, J. White, H. Orjuela, A. Bartolomucci, A. Eastman, S. Koul, K. Lebarbenchon, D. Bruhm, S. Short, K. Boyapati, N. Niknafs, C. Norton, V. Girish, N. Vulpescu, S. Velculescu, J. Velculescu, V. Adleff, A. Nelson, Z. Foda, B. Winterhoff, R. Drapkin, M. Schatz, J. Phallen, R. Scharpf, V. Velculescu
Somatic mosaicism contributes to genomic variation, yet postzygotic structural variants remain under-characterized. We performed long- and short-read WGS from multiple individuals (n=47 normal tissues; n=168 samples) and identified mosaic structural variants in all individuals and germ layers, impacting a median 285.2 kb/genome. Nearly half of breakpoints were independently validated, with tissue distributions reflecting both early and late developmental origins. Most mosaic variants were repeat-mediated and 8.3% overlapped functional elements, an enrichment compared to germline variants. To extend these analyses in samples where long-read sequencing is infeasible, we measured repeat alterations from short-read sequencing, recapitulating mosaic tissue-specific differences. We characterized tumor- and tissue- specific variation in repeats across 15 cancer types and found tumor-related repeat variation to be similar in scale to that of normal mosaic variation. Tracking repeat changes in cell-free DNA provided a noninvasive approach for tumor monitoring. Our analyses revealed widespread repeat-driven structural variation in health and disease.