Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1

Alexandra Tibelius; Joachim Marhold; Hanswalter Zentgraf; Christoph E Heilig; Heidemarie Neitzel; Bernard Ducommun; Anita Rauch; Anthony D Ho; Jiri Bartek; Alwin Krämer

doi:10.1083/jcb.200810159

Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1

Alexandra Tibelius, Joachim Marhold, Hanswalter Zentgraf, Christoph E Heilig, Heidemarie Neitzel, Bernard Ducommun, Anita Rauch, Anthony D Ho, Jiri Bartek, Alwin Krämer

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75 Citations (Scopus)

Abstract

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.

Original language	English
Journal	Journal of Cell Biology
Volume	185
Issue number	7
Pages (from-to)	1149-57
Number of pages	8
ISSN	0021-9525
DOIs	https://doi.org/10.1083/jcb.200810159
Publication status	Published - 2009

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title = "Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1",

abstract = "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.",

author = "Alexandra Tibelius and Joachim Marhold and Hanswalter Zentgraf and Heilig, {Christoph E} and Heidemarie Neitzel and Bernard Ducommun and Anita Rauch and Ho, {Anthony D} and Jiri Bartek and Alwin Kr{\"a}mer",

note = "Keywords: Animals; Antigens; Cell Line; Centrosome; Cyclin B; Enzyme Activation; Humans; Microcephaly; Mitosis; Nerve Tissue Proteins; Protein Kinases; RNA Interference; cdc25 Phosphatases",

year = "2009",

doi = "10.1083/jcb.200810159",

language = "English",

volume = "185",

pages = "1149--57",

journal = "Journal of Cell Biology",

issn = "0021-9525",

publisher = "Rockefeller University Press",

number = "7",

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TY - JOUR

T1 - Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1

AU - Tibelius, Alexandra

AU - Marhold, Joachim

AU - Zentgraf, Hanswalter

AU - Heilig, Christoph E

AU - Neitzel, Heidemarie

AU - Ducommun, Bernard

AU - Rauch, Anita

AU - Ho, Anthony D

AU - Bartek, Jiri

AU - Krämer, Alwin

N1 - Keywords: Animals; Antigens; Cell Line; Centrosome; Cyclin B; Enzyme Activation; Humans; Microcephaly; Mitosis; Nerve Tissue Proteins; Protein Kinases; RNA Interference; cdc25 Phosphatases

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

U2 - 10.1083/jcb.200810159

DO - 10.1083/jcb.200810159

M3 - Journal article

C2 - 19546241

SN - 0021-9525

VL - 185

SP - 1149

EP - 1157

JO - Journal of Cell Biology

JF - Journal of Cell Biology

IS - 7

ER -

Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1

Abstract

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