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Significance Chromosomal rearrangements are early and essential events in the formation of many tumors. Two distinct end-joining pathways, classic and alternative nonhomologous end joining, can mediate rearrangement formation. Previous studies have shown that genetic factors mediating rearrangements differ significantly between mouse and human cells. Here we show that poly(ADP)ribose polymerase 3 (Parp3) uniquely promotes chromosomal rearrangements in both species. Using next-generation sequencing of rearrangement junctions, we investigated the mechanistic contribution of Parp3 and a closely related enzyme, Parp1, that is also known to promote rearrangements in murine cells. We find differences in the phenotypes of rearrangements in cells lacking Parp3, Parp1, or both, suggesting that these enzymes promote rearrangements through distinct mechanisms and providing insight into this essential mechanism of tumorigenesis.

Parp3 promotes long-range end joining in murine cells