Nicholson, Joshua M.Macedo, Joana C.Mattingly, Aaron J.Wangsa, DarawaleeCamps, JordiLima, VeraGomes, Ana M.Doria, SofiaRied, ThomasLogarinho, ElsaCimini, Daniela2018-08-282018-08-282015-05-05http://hdl.handle.net/10919/84928Cancer cells display aneuploid karyotypes and typically mis-segregate chromosomes at high rates, a phenotype referred to as chromosomal instability (CIN). To test the effects of aneuploidy on chromosome segregation and other mitotic phenotypes we used the colorectal cancer cell line DLD1 (2n = 46) and two variants with trisomy 7 or 13 (DLD1+7 and DLD1+13), as well as euploid and trisomy 13 amniocytes (AF and AF+13). We found that trisomic cells displayed higher rates of chromosome mis-segregation compared to their euploid counterparts. Furthermore, cells with trisomy 13 displayed a distinctive cytokinesis failure phenotype. We showed that up-regulation of SPG20 expression, brought about by trisomy 13 in DLD1+13 and AF+13 cells, is sufficient for the cytokinesis failure phenotype. Overall, our study shows that aneuploidy can induce chromosome mis-segregation. Moreover, we identified a trisomy 13-specific mitotic phenotype that is driven by up-regulation of a gene encoded on the aneuploid chromosome.application/pdfen-USCreative Commons Attribution 4.0 InternationalCell biologyChromosomes and gene expressionAneuploidyCancerMis-segregationCytokinesisArticle - Refereedhttps://doi.org/10.7554/eLife.05068.0014