Mutational signatures reveal the role of RAD52 in p53-independent p21-driven genomic instability
Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21 WAF1/Cip1 , showing that its chronic expression...
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| Vydáno v: | Genome Biology Ročník 19; číslo 1; s. 37 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
16.03.2018
Springer Nature B.V BMC |
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| ISSN: | 1474-760X, 1474-7596, 1474-760X |
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| Abstract | Background
Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21
WAF1/Cip1
, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery.
Results
We now demonstrate that p21
WAF1/Cip1
can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation.
Conclusions
Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21
WAF1/Cip1
expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. |
|---|---|
| AbstractList | Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21WAF1/Cip1, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery. Results We now demonstrate that p21WAF1/Cip1 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation. Conclusions Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21WAF1/Cip1 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21WAF1/Cip1, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery.BACKGROUNDGenomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21WAF1/Cip1, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery.We now demonstrate that p21WAF1/Cip1 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation.RESULTSWe now demonstrate that p21WAF1/Cip1 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation.Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21WAF1/Cip1 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target.CONCLUSIONSOur results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21WAF1/Cip1 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21 WAF1/Cip1 , showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery. Results We now demonstrate that p21 WAF1/Cip1 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation. Conclusions Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21 WAF1/Cip1 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. BACKGROUND: Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21ᵂᴬF¹/Cⁱᵖ¹, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery. RESULTS: We now demonstrate that p21ᵂᴬF¹/Cⁱᵖ¹ can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation. CONCLUSIONS: Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21ᵂᴬF¹/Cⁱᵖ¹ expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21 , showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery. We now demonstrate that p21 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation. Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. Abstract Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic strategies. In a previous study, we reported an unexpected oncogenic property of p21WAF1/Cip1, showing that its chronic expression in a p53-deficient environment causes genomic instability by deregulation of the replication licensing machinery. Results We now demonstrate that p21WAF1/Cip1 can further fuel genomic instability by suppressing the repair capacity of low- and high-fidelity pathways that deal with nucleotide abnormalities. Consequently, fewer single nucleotide substitutions (SNSs) occur, while formation of highly deleterious DNA double-strand breaks (DSBs) is enhanced, crafting a characteristic mutational signature landscape. Guided by the mutational signatures formed, we find that the DSBs are repaired by Rad52-dependent break-induced replication (BIR) and single-strand annealing (SSA) repair pathways. Conversely, the error-free synthesis-dependent strand annealing (SDSA) repair route is deficient. Surprisingly, Rad52 is activated transcriptionally in an E2F1-dependent manner, rather than post-translationally as is common for DNA repair factor activation. Conclusions Our results signify the importance of mutational signatures as guides to disclose the repair history leading to genomic instability. We unveil how chronic p21WAF1/Cip1 expression rewires the repair process and identifies Rad52 as a source of genomic instability and a candidate therapeutic target. |
| ArticleNumber | 37 |
| Author | Swain, Umakanta Sørensen, Claus Storgaard Georgakilas, Alexandros G. Pappas, George Kotsinas, Athanassios Bartek, Jiri Souliotis, Vassilis L. Galanos, Panagiotis Polyzos, Alexander Lygerou, Zoi Glytsou, Christina Lukas, Jiri Lukas, Claudia Chowdhury, Dipanjan Scorrano, Luca Gorgoulis, Vassilis G. Svolaki, Ioanna Livneh, Zvi Giakoumakis, Nickolaos N. Geacintov, Nicholas Pateras, Ioannis S. |
| Author_xml | – sequence: 1 givenname: Panagiotis surname: Galanos fullname: Galanos, Panagiotis organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens, Danish Cancer Society Research Centre – sequence: 2 givenname: George surname: Pappas fullname: Pappas, George organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens, Danish Cancer Society Research Centre – sequence: 3 givenname: Alexander surname: Polyzos fullname: Polyzos, Alexander organization: Biomedical Research Foundation of the Academy of Athens – sequence: 4 givenname: Athanassios surname: Kotsinas fullname: Kotsinas, Athanassios organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens – sequence: 5 givenname: Ioanna surname: Svolaki fullname: Svolaki, Ioanna organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens – sequence: 6 givenname: Nickolaos N. surname: Giakoumakis fullname: Giakoumakis, Nickolaos N. organization: Laboratory of Biology, School of Medicine, University of Patras – sequence: 7 givenname: Christina surname: Glytsou fullname: Glytsou, Christina organization: Department of Biology, University of Padova – sequence: 8 givenname: Ioannis S. surname: Pateras fullname: Pateras, Ioannis S. organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens – sequence: 9 givenname: Umakanta surname: Swain fullname: Swain, Umakanta organization: Department of Biomolecular Sciences, Weizmann Institute of Science – sequence: 10 givenname: Vassilis L. surname: Souliotis fullname: Souliotis, Vassilis L. organization: Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation – sequence: 11 givenname: Alexandros G. surname: Georgakilas fullname: Georgakilas, Alexandros G. organization: Physics Department, School of Applied Mathematical and Physical Sciences, National Technical University of Athens (NTUA) – sequence: 12 givenname: Nicholas surname: Geacintov fullname: Geacintov, Nicholas organization: Department of Chemistry, New York University – sequence: 13 givenname: Luca surname: Scorrano fullname: Scorrano, Luca organization: Department of Biology, University of Padova – sequence: 14 givenname: Claudia surname: Lukas fullname: Lukas, Claudia organization: Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 15 givenname: Jiri surname: Lukas fullname: Lukas, Jiri organization: Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 16 givenname: Zvi surname: Livneh fullname: Livneh, Zvi organization: Department of Biomolecular Sciences, Weizmann Institute of Science – sequence: 17 givenname: Zoi surname: Lygerou fullname: Lygerou, Zoi organization: Laboratory of Biology, School of Medicine, University of Patras – sequence: 18 givenname: Dipanjan surname: Chowdhury fullname: Chowdhury, Dipanjan organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 19 givenname: Claus Storgaard surname: Sørensen fullname: Sørensen, Claus Storgaard organization: Biotech Research and Innovation Centre (BRIC), University of Copenhagen – sequence: 20 givenname: Jiri surname: Bartek fullname: Bartek, Jiri email: jb@cancer.dk organization: Danish Cancer Society Research Centre, Science for Life Laboratory, Division of Genome Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institute – sequence: 21 givenname: Vassilis G. surname: Gorgoulis fullname: Gorgoulis, Vassilis G. email: vgorg@med.uoa.gr, vgorgoulis@gmail.com organization: Molecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National Kapodistrian University of Athens, Biomedical Research Foundation of the Academy of Athens, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29548335$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:137872724$$DView record from Swedish Publication Index (Karolinska Institutet) |
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| Keywords | Single nucleotide substitution (SNS) Rad52 Single strand annealing (SSA) Translesion DNA synthesis (TLS) Break-induced replication (BIR) p21 Genomic instability p21WAF1/Cip1 |
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| License | Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
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Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate... Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate therapeutic... Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate... BACKGROUND: Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of appropriate... Abstract Background Genomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential for the design of... |
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| SubjectTerms | Animal Genetics and Genomics Bioinformatics Biomedical and Life Sciences Break-induced replication (BIR) Cancer Cell Line Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - metabolism Deoxyribonucleic acid DNA DNA - biosynthesis DNA damage DNA Repair evolution Evolutionary Biology Experiments fuels genetic instability genome Genomes Genomic Instability Human Genetics Humans Irritable bowel syndrome landscapes Life Sciences Microbial Genetics and Genomics Mutation p21WAF1/Cip1 p53 Protein Plant Genetics and Genomics Post-translation Rad52 Rad52 DNA Repair and Recombination Protein - physiology Rad52 protein Recruitment Replication Senescence Signatures Single nucleotide substitution (SNS) Therapeutic applications therapeutics Transcription transcription (genetics) Translesion DNA synthesis (TLS) Tumor Suppressor Protein p53 - physiology Tumors |
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| Title | Mutational signatures reveal the role of RAD52 in p53-independent p21-driven genomic instability |
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