 Hi, I'm Lucine Nazarian Peterson, the first author of the article entitled German Chromotrypsis Driven by L1 Made Datives Retrotransposition and Allualdo Homologous Recombination. Together with my colleagues and collaborators, we published this article in the Journal of Human Mutation. Chromotrypsis is a phenomenon of chromosome shattering by unknown intra or extracellular factors where hundreds of DNA double strand breaks are localized in relatively small genomic regions ranging from a few hundred kilobase up to several megabase in size or in larger regions as whole chromosome arms or even entire chromosomes. These generated double strand breaks are subsequently stitched together in a random order and result in complex genomic and chromosomal rearrangements. Chromotrypsis was first characterized in cancer but soon after it was also detected in congenital and developmental disorders and first term germline chromotrypsis. The breakpoint junction sequence features of until now described relatively balanced chromotrypsis cases suggest that the multiple double strand breaks are joined together by non-homologous and joining or micro-homology mediated and joining repair mechanisms. Until now no homologous sequences have been reported which suggested that non-allelic homologous recombination is rather excluded from chromotrypsis. Although the DNA repair mechanism involved in chromotrypsis have been described the mechanism driving the localized shattering process remain unclear. In this study we analyzed the breakpoint junction sequences of germline chromotrypsis involving chromosomes 3 and 5. An approximately 6.4 megabase region at chromosome 3 was shattered by 6 DNA breaks generating 7 fragments named 3A23G while chromosome 5 had a single breakpoint. In addition at chromosome 3 an approximately 110 kilobase deletion was detected that was fragment 3C. What is interesting in our study is that for the first time we identified Alu elements at 4 of the 7 breakpoint sequences of these germline chromotrypsis. Alu elements are approximately 300 base pair active primate specific signed retro transposons and due to their high copy number these elements are prone to non-allelic homologous recombination. Such events have resulted in benign and pathogenic genomic deletions duplications and inversions in humans. The two Alu-SX elements flanking the 100 kV deleted 3C fragment are in the same orientation. Yet two other Alu elements spanning the breakpoints of the fragment 3E are from different sub-families Alu-SQ and Alu-JB and are in opposite orientation. Our second very interesting observation in this study is that it's the inserted 502 base pair sequence at the breakpoint 3C 3D. Blood search of this sequence showed that it shared 100% nucleotide identity to a full length SVA element located on chromosome 7 belonging to a known active sub-familie SVAe. Our analysis revealed that this inserted SVA element displaced characteristics of L1 mediated retrotransposition specifically because the 5' end of SVAe element was truncated and the insertion occurred within a sequence resembling the L1 endonuclease cleavage site, TTT, TGA. Our analysis suggests that the SVAe insertion did not occur prior to or after but concurrent with the chromatripsis event. We also observed L1 endonuclease potential target sites in other breakpoints at chromosome 3 and therefore we suggest that chromatin looping which is shown in this figure mediated by homologous Alu elements may have brought distal DNA regions into close proximity facilitating DNA cleavage by catalytically active L1 endonuclease. Thus we propose the model, the details of what are presented in this figure. In conclusion, are there to provide the first evidence that active and inactive human retrotransposants can serve as endogenous motogens driving chromatripsis in the germline?