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Published online
doi:10.1083/jcb.200810159
The Journal of Cell Biology, Vol. 185, No. 7, 1149-1157
The Rockefeller University Press, 0021-9525 $30.00
© Tibelius et al.
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Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1



Alexandra Tibelius1,3, Joachim Marhold1,3, Hanswalter Zentgraf2, Christoph E. Heilig1,3, Heidemarie Neitzel4, Bernard Ducommun5, Anita Rauch6, Anthony D. Ho3, Jiri Bartek7, and Alwin Krämer1,3

1 Clinical Cooperation Unit Molecular Hematology/Oncology and 2 Department of Tumor Virology, German Cancer Research Center, 69120 Heidelberg, Germany
3 Department of Internal Medicine V, University of Heidelberg, 69120 Heidelberg, Germany
4 Institute of Human Genetics, Charité, University of Berlin, 14195 Berlin, Germany
5 Laboratoire de Biologie Cellulaire et Moléculaire du Controle de la Prolifération, Centre National de la Recherche Scientifique, 31062 Toulouse, France
6 Institute of Human Genetics, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany
7 Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, 2100 Copenhagen, Denmark

Correspondence to Alwin Krämer: a.kraemer{at}dkfz.de

Primary microcephaly, Seckel syndrome, and microcephalic osteodysplastic primordial dwarfism type II (MOPD II) are disorders exhibiting marked microcephaly, with small brain sizes reflecting reduced neuron production during fetal life. Although primary microcephaly can be caused by mutations in microcephalin (MCPH1), cells from patients with Seckel syndrome and MOPD II harbor mutations in ataxia telangiectasia and Rad3 related (ATR) or pericentrin (PCNT), leading to disturbed ATR signaling. In this study, we show that a lack of MCPH1 or PCNT results in a loss of Chk1 from centrosomes with subsequently deregulated activation of centrosomal cyclin B–Cdk1.

Abbreviations used in this paper: ATR, ataxia telangiectasia and Rad3 related; LBC, lymphoblastoid cell; MCPH1, microcephalin; MOPD II, microcephalic osteodysplastic primordial dwarfism type II; PACT, PCNT-AKAP450 centrosomal targeting; PCC, premature chromosome condensation; PCNT, pericentrin.

© 2009 Tibelius et al.
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