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Securin is not required for chromosomal stability in human cells.
PLoS Biol. 3, 2127-2134:e416 (2005)
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.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
SISTER-CHROMATID SEPARATION; ANAPHASE; COHESION; PHOSPHORYLATION; IDENTIFICATION; INHIBITION; METAPHASE; CLEAVAGE; YEAST; HPTTG
ISSN (print) / ISBN
1544-9173
e-ISSN
1545-7885
Zeitschrift
PLoS Biology
Quellenangaben
Band: 3,
Heft: 12,
Seiten: 2127-2134,
Artikelnummer: e416
Verlag
Public Library of Science (PLoS)
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Human Genetics (IHG)