High Multiplex Translocation sequencing (HMTS) detect translocation in MCF7 and HEK293T with different treatments and in NCAPH2 deficinecy cells treated with ETO.

To tackle this challenge, we devised a strategy to detect and enrich cells with translocations in vitro, in conjunction with a novel method termed High Multiplex Translocation Sequencing (HMTS), to capture genome-wide translocations from multiple bait regions simultaneously.

Analysis of HMTS data unveiled a tendency for translocations to occur at Topologically Associating Domain (TAD) boundaries, and experimental disruption of the TAD boundary indeed led to a reduction in translocation frequency, exemplified by translocations involving ERG. Using HMTS, condensin II were found to play a role in facilitating translocations, and condensin II deficiency inhibited long-distance TAD boundary translocations in G1.