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Journal Article

Securin Is Not Required for Chromosomal Stability in Human Cells

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78102

Heubes,  Simone
Jentsch, Stefan / Molecular Cell Biology, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78750

Stemmann,  Olaf
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

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PLoS_Biol_3(12)_e416.pdf
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Citation

Pfleghaar, K., Heubes, S., Cox, J., Stemmann, O., & Speicher, M. R. (2005). Securin Is Not Required for Chromosomal Stability in Human Cells. PLoS Biology, 3(12): e416. doi:10.1371/journal.pbio.0030416.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-67D3-A
Abstract
Abnormalities of chromosome number are frequently observed in cancers. The mechanisms regulating chromosome segregation in human cells are therefore of great interest. Recently it has been reported that human cells without an hSecurin gene lose chromosomes at a high frequency. Here we show that, after hSecurin knockout through homologous recombination, chromosome losses are only a short, transient effect. After a few passages hSecurin−/− cells became chromosomally stable and executed mitoses normally. This was unexpected, as the securin loss resulted in a persisting reduction of the sister-separating protease separase and inefficient cleavage of the cohesin subunit Scc1. Our data demonstrate that securin is dispensable for chromosomal stability in human cells. We propose that human cells possess efficient mechanisms to compensate for the loss of genes involved in chromosome segregation.