Ectopic expression of meiotic cohesin generates chromosome instability in cancer cell line

This work originated from mining of cancer genome data and proceeded to analyze the effects of ectopic expression of meiotic cohesins in mitotic cells in culture. In the process, apart from conclusively answering the question on mechanisms for RAD21L toxicity and its underrepresentation in tumor transcriptomes, we found an association of meiotic cohesin binding with BORIS/CTCFL sites in the normal testis. We also elucidated the patterns and outcomes of meiotic cohesin binding to chromosomes in model cell lines. Furthermore, we uncovered that RAD21L-based meiotic cohesin possesses a self-contained chromosome restructuring activity able to trigger sustainable but imperfect mitotic arrest leading to chromosomal instability. The discovered epigenomic and genetic mechanisms can be relevant to chromosome instability in cancer.