NDLI: Inactivation of Cdc7 kinase in mouse ES cells results in S-phase arrest and p53-dependent cell death

Content Provider	PubMed Central
Author	Kim, Jung Min Nakao, Kazuki Nakamura, Kenji Saito, Izumu Katsuki, Motoya Arai, Ken-ichi Masai, Hisao
Copyright Year	2002
Abstract	Cdc7-related kinases play essential roles in the initiation of yeast DNA replication. We show that mice lacking murine homologs of Cdc7 (muCdc7) genes die between E3.5 and E6.5. We have established a mutant embryonic stem (ES) cell line lacking the muCdc7 genes in the presence of a loxP-flanked transgene expressing muCdc7 cDNA. Upon removal of the transgene by Cre recombinase, mutant ES cells cease DNA synthesis, arresting growth with S-phase DNA content, and generate nuclear Rad51 foci, followed by cell death with concomitant increase in p53 protein levels. Inhibition of p53 leads to partial rescue of muCdc7–/– ES cells from cell death. muCdc7–/–p53–/– embryos survive up to E8.5, and their blastocysts generate inner cell mass of a significant size in vitro, whereas those of the muCdc7–/–p53+/– embryos undergoes complete degeneration. These results demonstrate that, in contrast to cell cycle arrest at the G1/S boundary observed in yeasts, loss of Cdc7 in ES cells results in rapid cessation of DNA synthesis within S phase, triggering checkpoint responses leading to recombinational repair and p53-dependent cell death.
Related Links	http://dx.doi.org/10.1093/emboj/21.9.2168
Ending Page	2179
Page Count	12
Starting Page	2168
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	9
Volume Number	21
Language	English
Publisher	Oxford University Press
Publisher Date	2002-05-01
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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