DNA damage bypass operates in the S and G2 phases of the cell cycle and exhibits differential mutagenicity

Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-i...

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Published in:	Nucleic acids research Vol. 40; no. 1; pp. 170 - 180
Main Authors:	Diamant, Noam, Hendel, Ayal, Vered, Ilan, Carell, Thomas, Reißner, Thomas, de Wind, Niels, Geacinov, Nicholas, Livneh, Zvi
Format:	Journal Article
Language:	English
Published:	England Oxford University Press 01.01.2012
Subjects:	Animals Cell Line, Tumor Cells, Cultured DNA - biosynthesis DNA Damage DNA-Binding Proteins - physiology DNA-Directed DNA Polymerase - physiology G2 Phase - genetics Genome Integrity, Repair and Humans Mice Mutagenesis Nuclear Proteins - physiology Nucleotidyltransferases - physiology Replication Protein A - analysis S Phase - genetics Ultraviolet Rays
ISSN:	0305-1048, 1362-4962, 1362-4962
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Abstract	Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-irradiated mammalian cells, chromosomal single-stranded gaps formed in S phase during replication persist into the G2 phase of the cell cycle, where their repair is completed depending on DNA polymerase ζ and Rev1. Analysis of TLS using a high-resolution gapped-plasmid assay system in cell populations enriched by centrifugal elutriation for specific cell cycle phases showed that TLS operates both in S and G2. Moreover, the mutagenic specificity of TLS in G2 was different from S, and in some cases overall mutation frequency was higher. These results suggest that TLS repair of single-stranded gaps caused by DNA lesions can lag behind chromosomal replication, is separable from it, and occurs both in the S and G2 phases of the cell cycle. Such a mechanism may function to maintain efficient replication, which can progress despite the presence of DNA lesions, with TLS lagging behind and patching regions of discontinuity.
AbstractList	Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-irradiated mammalian cells, chromosomal single-stranded gaps formed in S phase during replication persist into the G2 phase of the cell cycle, where their repair is completed depending on DNA polymerase ζ and Rev1. Analysis of TLS using a high-resolution gapped-plasmid assay system in cell populations enriched by centrifugal elutriation for specific cell cycle phases showed that TLS operates both in S and G2. Moreover, the mutagenic specificity of TLS in G2 was different from S, and in some cases overall mutation frequency was higher. These results suggest that TLS repair of single-stranded gaps caused by DNA lesions can lag behind chromosomal replication, is separable from it, and occurs both in the S and G2 phases of the cell cycle. Such a mechanism may function to maintain efficient replication, which can progress despite the presence of DNA lesions, with TLS lagging behind and patching regions of discontinuity. Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-irradiated mammalian cells, chromosomal single-stranded gaps formed in S phase during replication persist into the G2 phase of the cell cycle, where their repair is completed depending on DNA polymerase ζ and Rev1. Analysis of TLS using a high-resolution gapped-plasmid assay system in cell populations enriched by centrifugal elutriation for specific cell cycle phases showed that TLS operates both in S and G2. Moreover, the mutagenic specificity of TLS in G2 was different from S, and in some cases overall mutation frequency was higher. These results suggest that TLS repair of single-stranded gaps caused by DNA lesions can lag behind chromosomal replication, is separable from it, and occurs both in the S and G2 phases of the cell cycle. Such a mechanism may function to maintain efficient replication, which can progress despite the presence of DNA lesions, with TLS lagging behind and patching regions of discontinuity.Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-irradiated mammalian cells, chromosomal single-stranded gaps formed in S phase during replication persist into the G2 phase of the cell cycle, where their repair is completed depending on DNA polymerase ζ and Rev1. Analysis of TLS using a high-resolution gapped-plasmid assay system in cell populations enriched by centrifugal elutriation for specific cell cycle phases showed that TLS operates both in S and G2. Moreover, the mutagenic specificity of TLS in G2 was different from S, and in some cases overall mutation frequency was higher. These results suggest that TLS repair of single-stranded gaps caused by DNA lesions can lag behind chromosomal replication, is separable from it, and occurs both in the S and G2 phases of the cell cycle. Such a mechanism may function to maintain efficient replication, which can progress despite the presence of DNA lesions, with TLS lagging behind and patching regions of discontinuity.
Author	Diamant, Noam Vered, Ilan Reißner, Thomas Carell, Thomas Hendel, Ayal Livneh, Zvi Geacinov, Nicholas de Wind, Niels
AuthorAffiliation	1 Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2 Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3 Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4 Department of Chemistry, New York University, New York, NY 10003-5180, USA
AuthorAffiliation_xml	– name: 1 Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2 Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3 Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4 Department of Chemistry, New York University, New York, NY 10003-5180, USA
Author_xml	– sequence: 1 givenname: Noam surname: Diamant fullname: Diamant, Noam organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 2 givenname: Ayal surname: Hendel fullname: Hendel, Ayal organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 3 givenname: Ilan surname: Vered fullname: Vered, Ilan organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 4 givenname: Thomas surname: Carell fullname: Carell, Thomas organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 5 givenname: Thomas surname: Reißner fullname: Reißner, Thomas organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 6 givenname: Niels surname: de Wind fullname: de Wind, Niels organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 7 givenname: Nicholas surname: Geacinov fullname: Geacinov, Nicholas organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA – sequence: 8 givenname: Zvi surname: Livneh fullname: Livneh, Zvi email: zvi.livneh@weizmann.ac.il organization: 1Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel, 2Department of Chemistry and Biochemistry, Ludwig-Maximilians-University Munich, 81377 München, Germany, 3Department of Toxicogenetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands and 4Department of Chemistry, New York University, New York, NY 10003-5180, USA
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Snippet	Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication...
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SubjectTerms	Animals Cell Line, Tumor Cells, Cultured DNA - biosynthesis DNA Damage DNA-Binding Proteins - physiology DNA-Directed DNA Polymerase - physiology G2 Phase - genetics Genome Integrity, Repair and Humans Mice Mutagenesis Nuclear Proteins - physiology Nucleotidyltransferases - physiology Replication Protein A - analysis S Phase - genetics Ultraviolet Rays
Title	DNA damage bypass operates in the S and G2 phases of the cell cycle and exhibits differential mutagenicity
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