1. ¹Department of Radiation and Stress Cell Biology, University of Groningen, UMCG, Ant. Deusinglaan 1, 9713 AV Groningen, The Netherlands
2. ²Department of Reproduction and Development, Faculty of Medicine and Health Sciences, Erasmus University of Rotterdam, Rotterdam, The Netherlands

Correspondence: OCM Sibon, E-mail: o.c.m.sibon@med.umcg.nl

³These authors contributed equally to this work

Received 29 October 2004; Revised 3 May 2005; Accepted 12 May 2005; Published online 3 October 2005.

Abstract

A remarkable and yet unexplained phenomenon in cancer cells is the presence of multiple centrosomes, organelles required for normal cell division. Previously, it was demonstrated that the tumor suppressor BRCA1 is a component of centrosomes. This observation led to the hypothesis that defective BRCA1 results in malfunctioning centrosomes and faulty centrosomes are a possible cause of cancer. Using EGFP-tagged fusion proteins and BRCA1^-/- cells we show that although some BRCA1 antibodies do label centrosomes under certain fixation conditions, BRCA1 is not a centrosomal protein. Therefore, it is unlikely that a mutation in BRCA1 directly alters centrosome structure and function. BRCA1 plays an established role in DNA damage repair and in G₂/M checkpoint regulation. We present evidence that multiple centrosomes can arise in any cell when G₂/M checkpoint fails and entrance into mitosis occurs in the presence of DNA damage.