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

ABSTRACT: Chromosomal translocations play pivotal roles in various physiological and pathological processes, such as immunoglobulin production and tumor progression; however, the infrequency of chromosomal translocation events has impeded the exploration of the underlying mechanisms. 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. Intriguingly, in contrast, condensin II deficiency decreased intra-chromatin translocation at TAD boundaries but paradoxically globally increased inter-chromatin translocation frequency, suggesting that condensin II physiologically restricts certain chromatin interactions to prevent translocations. One significant role of condensin II in maintaining chromosome territorial architecture may be to prevent inter-chromatin translocation, thereby safeguarding the genome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268011 | GEO | 2026/05/21

REPOSITORIES: GEO