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      Arabidopsis R1R2R3-Myb proteins are essential for inhibiting cell division in response to DNA damage

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          Abstract

          Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity. However, how DNA damage arrests the plant cell cycle is largely unknown. Here, we show that the repressor-type R1R2R3-Myb transcription factors (Rep-MYBs), which suppress G2/M-specific genes, are required to inhibit cell division in response to DNA damage. Knockout mutants are resistant to agents that cause DNA double-strand breaks and replication stress. Cyclin-dependent kinases (CDKs) can phosphorylate Rep-MYBs in vitro and are involved in their proteasomal degradation. DNA damage reduces CDK activities and causes accumulation of Rep-MYBs and cytological changes consistent with cell cycle arrest. Our results suggest that CDK suppressors such as CDK inhibitors are not sufficient to arrest the cell cycle in response to DNA damage but that Rep-MYB-dependent repression of G2/M-specific genes is crucial, indicating an essential function for Rep-MYBs in the DNA damage response.

          Abstract

          Inhibition of cell division maintains genome integrity in response to DNA damage. Here Chen et al. propose that DNA damage causes cell cycle arrest in the Arabidopsis root via Rep-MYB transcription factor-mediated repression of G2/M-specific gene expression in response to reduced cyclin-dependent kinase activity.

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          The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer.

          Joanne Smith, Lye Tho, Naihan Xu … (2010)
          DNA damage is a key factor both in the evolution and treatment of cancer. Genomic instability is a common feature of cancer cells, fuelling accumulation of oncogenic mutations, while radiation and diverse genotoxic agents remain important, if imperfect, therapeutic modalities. Cellular responses to DNA damage are coordinated primarily by two distinct kinase signaling cascades, the ATM-Chk2 and ATR-Chk1 pathways, which are activated by DNA double-strand breaks (DSBs) and single-stranded DNA respectively. Historically, these pathways were thought to act in parallel with overlapping functions; however, more recently it has become apparent that their relationship is more complex. In response to DSBs, ATM is required both for ATR-Chk1 activation and to initiate DNA repair via homologous recombination (HRR) by promoting formation of single-stranded DNA at sites of damage through nucleolytic resection. Interestingly, cells and organisms survive with mutations in ATM or other components required for HRR, such as BRCA1 and BRCA2, but at the cost of genomic instability and cancer predisposition. By contrast, the ATR-Chk1 pathway is the principal direct effector of the DNA damage and replication checkpoints and, as such, is essential for the survival of many, although not all, cell types. Remarkably, deficiency for HRR in BRCA1- and BRCA2-deficient tumors confers sensitivity to cisplatin and inhibitors of poly(ADP-ribose) polymerase (PARP), an enzyme required for repair of endogenous DNA damage. In addition, suppressing DNA damage and replication checkpoint responses by inhibiting Chk1 can enhance tumor cell killing by diverse genotoxic agents. Here, we review current understanding of the organization and functions of the ATM-Chk2 and ATR-Chk1 pathways and the prospects for targeting DNA damage signaling processes for therapeutic purposes. Copyright © 2010 Elsevier Inc. All rights reserved.
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            The MuvB complex sequentially recruits B-Myb and FoxM1 to promote mitotic gene expression.

            James DeCaprio, Subhashini Sadasivam, S.-H. Duan (2012)
            Cell cycle progression is dependent on two major waves of gene expression. Early cell cycle gene expression occurs during G1/S to generate factors required for DNA replication, while late cell cycle gene expression begins during G2 to prepare for mitosis. Here we demonstrate that the MuvB complex-comprised of LIN9, LIN37, LIN52, LIN54, and RBBP4-serves an essential role in three distinct transcription complexes to regulate cell cycle gene expression. The MuvB complex, together with the Rb-like protein p130, E2F4, and DP1, forms the DREAM complex during quiescence and represses expression of both early and late genes. Upon cell cycle entry, the MuvB complex dissociates from p130/DREAM, binds to B-Myb, and reassociates with the promoters of late genes during S phase. MuvB and B-Myb are required for the subsequent recruitment of FoxM1 to late gene promoters during G2. The MuvB complex remains bound to FoxM1 during peak late cell cycle gene expression, while B-Myb binding is lost when it undergoes phosphorylation-dependent, proteasome-mediated degradation during late S phase. Our results reveal a novel role for the MuvB complex in recruiting B-Myb and FoxM1 to promote late cell cycle gene expression and in regulating cell cycle gene expression from quiescence through mitosis.
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              ATR and ATM play both distinct and additive roles in response to ionizing radiation.

              Julia Foreman, Charles E. Robertson, Kevin M. Culligan … (2006)
              The ATR and ATM protein kinases are known to be involved in a wide variety of responses to DNA damage. The Arabidopsis thaliana genome includes both ATR and ATM orthologs, and plants with null alleles of these genes are viable. Arabidopsis atr and atm mutants display hypersensitivity to gamma-irradiation. To further characterize the roles of ATM and ATR in response to ionizing radiation, we performed a short-term global transcription analysis in wild-type and mutant lines. We found that hundreds of genes are upregulated in response to gamma-irradiation, and that the induction of virtually all of these genes is dependent on ATM, but not ATR. The transcript of CYCB1;1 is unique among the cyclin transcripts in being rapidly and powerfully upregulated in response to ionizing radiation, while other G(2)-associated transcripts are suppressed. We found that both ATM and ATR contribute to the induction of a CYCB1;1:GUS fusion by IR, but only ATR is required for the persistence of this response. We propose that this upregulation of CYCB1;1 does not reflect the accumulation of cells in G(2), but instead reflects a still unknown role for this cyclin in DNA damage response.
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                Author and article information

                Contributors
                Masaaki Umeda: mumeda@bs.naist.jp
                Journal
                Journal ID (nlm-ta): Nat Commun
                Journal ID (iso-abbrev): Nat Commun
                Title: Nature Communications
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-1723
                Publication date (Electronic): 21 September 2017
                Publication date PMC-release: 21 September 2017
                Publication date Collection: 2017
                Volume: 8
                Electronic Location Identifier: 635
                Affiliations
                [1 ]ISNI 0000 0000 9227 2257, GRID grid.260493.a, Graduate School of Biological Sciences, , Nara Institute of Science and Technology, ; Takayama 8916-5, Ikoma, Nara 630-0192 Japan
                [2 ]ISNI 0000 0000 8863 9909, GRID grid.262576.2, Department of Bioinformatics, , Ritsumeikan University, ; Kusatsu, Shiga 525-8577 Japan
                [3 ]ISNI 0000 0001 0943 978X, GRID grid.27476.30, Graduate School of Bioagricultural Sciences, , Nagoya University, ; Chikusa, Nagoya 464-8601 Japan
                [4 ]ISNI 0000 0004 1754 9200, GRID grid.419082.6, JST, , CREST, ; Chikusa, Nagoya 464-8601 Japan
                [5 ]ISNI 0000 0004 1754 9200, GRID grid.419082.6, JST, , CREST, ; Takayama 8916-5, Ikoma, Nara 630-0192 Japan
                Article
                Publisher ID: 676
                DOI: 10.1038/s41467-017-00676-4
                PMC ID: 5608833
                PubMed ID: 28935922
                SO-VID: 3bf2afab-3293-4246-bf10-eb2aeab6c053
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 11 March 2016
                Date accepted : 19 July 2017
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

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