Published in

Public Library of Science, PLoS Biology, 12(3), p. e416, 2005

DOI: 10.1371/journal.pbio.0030416

Links

Tools

Export citation

Search in Google Scholar

Securin Is Not Required for Chromosomal Stability in Human Cells

Journal article published in 2005 by Katrin Pfleghaar, Simone Heubes, Jürgen Cox, Olaf Stemmann, Michael R. Speicher ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Green circle
Preprint: archiving allowed
Upload
Green circle
Postprint: archiving allowed
Upload
Green circle
Published version: archiving allowed
Upload
Policy details
Data provided by SHERPA/RoMEO

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.