Chromosome mis-segregation and cytokinesis failure in trisomic human cells

• Type: Article in International Scientific Journal
• Date: 2015

Authors

Nicholson, JM (Author) Other; Macedo, JC (Author) Other; Mattingly, AJ (Author) Other; Wangsa, D (Author) Other; Camps, J (Author) Other; Lima, V (Author) FMUP; Gomes, AM (Author) Other; doria, s (Author) FMUP; Ried, T (Author) Other; Logarinho, E (Author) Other; Cimini, D (Author) Other

Journal

Title: eLife

Vol. 4

ISSN: 2050-084X

Publisher: eLife Sciences Publications

Indexing

ISI Web of Knowledge - 80 Citations

Scopus - 76 Citations

Other information

Authenticus ID: P-00G-B15

DOI: 10.7554/elife.05068

Abstract (EN): Cancer 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 23