Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates

Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E an...

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Vydané v:	The Journal of cell biology Ročník 200; číslo 6; s. 699
Hlavní autori:	Neelsen, Kai J, Zanini, Isabella M Y, Herrador, Raquel, Lopes, Massimo
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 18.03.2013
Predmet:	CDC2 Protein Kinase - genetics CDC2 Protein Kinase - metabolism cdc25 Phosphatases - genetics cdc25 Phosphatases - metabolism Cell Line, Tumor Chromosome Breakage Cyclin E - genetics Cyclin E - metabolism DNA Replication DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Endonucleases - genetics Endonucleases - metabolism G2 Phase Humans Mitosis Oncogenes
ISSN:	1540-8140, 1540-8140
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Abstract	Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E and Cdc25A rapidly slowed down replication forks and induced fork reversal, suggestive of increased topological stress. Surprisingly, these phenotypes, per se, are neither associated with chromosomal breakage nor with significant DDR activation. Oncogene-induced DNA breakage and DDR activation instead occurred upon persistent G2/M arrest or, in a checkpoint-defective context, upon premature CDK1 activation. Depletion of MUS81, a cell cycle-regulated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed forks. We propose that nucleolytic processing of unusual replication intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosis is a central anti-tumorigenic function of the DNA damage checkpoints.
AbstractList	Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E and Cdc25A rapidly slowed down replication forks and induced fork reversal, suggestive of increased topological stress. Surprisingly, these phenotypes, per se, are neither associated with chromosomal breakage nor with significant DDR activation. Oncogene-induced DNA breakage and DDR activation instead occurred upon persistent G2/M arrest or, in a checkpoint-defective context, upon premature CDK1 activation. Depletion of MUS81, a cell cycle-regulated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed forks. We propose that nucleolytic processing of unusual replication intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosis is a central anti-tumorigenic function of the DNA damage checkpoints.Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E and Cdc25A rapidly slowed down replication forks and induced fork reversal, suggestive of increased topological stress. Surprisingly, these phenotypes, per se, are neither associated with chromosomal breakage nor with significant DDR activation. Oncogene-induced DNA breakage and DDR activation instead occurred upon persistent G2/M arrest or, in a checkpoint-defective context, upon premature CDK1 activation. Depletion of MUS81, a cell cycle-regulated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed forks. We propose that nucleolytic processing of unusual replication intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosis is a central anti-tumorigenic function of the DNA damage checkpoints. Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E and Cdc25A rapidly slowed down replication forks and induced fork reversal, suggestive of increased topological stress. Surprisingly, these phenotypes, per se, are neither associated with chromosomal breakage nor with significant DDR activation. Oncogene-induced DNA breakage and DDR activation instead occurred upon persistent G2/M arrest or, in a checkpoint-defective context, upon premature CDK1 activation. Depletion of MUS81, a cell cycle-regulated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed forks. We propose that nucleolytic processing of unusual replication intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosis is a central anti-tumorigenic function of the DNA damage checkpoints.
Author	Zanini, Isabella M Y Lopes, Massimo Neelsen, Kai J Herrador, Raquel
Author_xml	– sequence: 1 givenname: Kai J surname: Neelsen fullname: Neelsen, Kai J organization: Institute of Molecular Cancer Research, University of Zurich, CH-8057 Zurich, Switzerland – sequence: 2 givenname: Isabella M Y surname: Zanini fullname: Zanini, Isabella M Y – sequence: 3 givenname: Raquel surname: Herrador fullname: Herrador, Raquel – sequence: 4 givenname: Massimo surname: Lopes fullname: Lopes, Massimo
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Snippet	Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes...
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SubjectTerms	CDC2 Protein Kinase - genetics CDC2 Protein Kinase - metabolism cdc25 Phosphatases - genetics cdc25 Phosphatases - metabolism Cell Line, Tumor Chromosome Breakage Cyclin E - genetics Cyclin E - metabolism DNA Replication DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Endonucleases - genetics Endonucleases - metabolism G2 Phase Humans Mitosis Oncogenes
Title	Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates
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