Genomic Instability and Endoreduplication Triggered by RAD17 Deletion
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Plasticity in Ploidy: a Generalized Response to Stress
Review Plasticity in ploidy: a generalized response to stress Daniel R. Scholes and Ken N. Paige School of Integrative Biology, University of Illinois at Urbana-Champaign, 515 Morrill Hall, 505 South Goodwin Avenue, Urbana, IL 61801, USA Endoreduplication, the replication of the genome with- or greater) are a general feature of endosperm and sus- out mitosis, leads to an increase in the cellular ploidy of pensor cells of seed across endopolyploid taxa [9]. Very low an organism over its lifetime, a condition termed ‘endo- (or the complete lack of) endopolyploidy across taxa is polyploidy’. Endopolyploidy is thought to play signifi- observed in a few cell types, including phloem companion cant roles in physiology and development through cells and stomatal guard cells, both of which serve highly cellular, metabolic, and genetic effects. While the occur- specialized functions that would possibly be disrupted by rence of endopolyploidy has been observed widely increased ploidy [7,9]. Because endoreduplication is a across taxa, studies have only recently begun to charac- somatic process, the embryo and meristematic cells terize and manipulate endopolyploidy with a focus on its (e.g., procambium, root and shoot apical meristems) also ecological and evolutionary importance. No compilation lack endopolyploidy [6,7,9]. Finally, mixed ploidy among of these examples implicating endoreduplication as a adjacent cells of the same type also occurs (e.g., leaf generalized response to stress has thus far been made, epidermal pavement cells range from 2C to 64C) [7,9]. despite the growing evidence supporting this notion. Although generalized patterns of endopolyploidy may We review here the recent literature of stress-induced be observed within and among plants, recent evidence endopolyploidy and suggest that plants employ endor- suggests that many plants that endoreduplicate can plas- eduplication as an adaptive, plastic response to mitigate tically increase their endopolyploidy beyond their ‘normal’ the effects of stress. -
Cell Cycle Arrest and DNA Endoreduplication Following P21waf1/Cip1 Expression
Oncogene (1998) 17, 1691 ± 1703 1998 Stockton Press All rights reserved 0950 ± 9232/98 $12.00 http://www.stockton-press.co.uk/onc Cell cycle arrest and DNA endoreduplication following p21Waf1/Cip1 expression Stewart Bates, Kevin M Ryan, Andrew C Phillips and Karen H Vousden ABL Basic Research Program, NCI-FCRDC, Building 560, Room 22-96, West 7th Street, Frederick, Maryland 21702-1201, USA p21Waf1/Cip1 is a major transcriptional target of p53 and there are an increasing number of regulatory mechan- has been shown to be one of the principal mediators of isms that serve to inhibit cdk activity. Primary amongst the p53 induced G1 cell cycle arrest. We show that in these is the expression of cdk inhibitors (CDKIs) that addition to the G1 block, p21Waf1/Cip1 can also contribute can bind to and inhibit cyclin/cdk complexes (Sherr to a delay in G2 and expression of p21Waf1/Cip1 gives rise and Roberts, 1996). These fall into two classes, the to cell cycle pro®les essentially indistinguishable from INK family which bind to cdk4 and cdk6 and inhibit those obtained following p53 expression. Arrest of cells complex formation with D-cyclins, and the p21Waf1/Cip1 in G2 likely re¯ects an inability to induce cyclin B1/cdc2 family that bind to cyclin/cdk complexes and inhibit kinase activity in the presence of p21Waf1/Cip1, although the kinase activity. inecient association of p21Waf1/Cip1 and cyclin B1 The p21Waf1/Cip1 family of CDKIs include p21Waf1/Cip1, suggests that the mechanism of inhibition is indirect. p27 and p57 and are broad range inhibitors of cyclin/ Cells released from an S-phase block were not retarded cdk complexes (Gu et al., 1993; Harper et al., 1993; in their ability to progress through S-phase by the Xiong et al., 1993; Firpo et al., 1994; Polyak et al., presence of p21Waf1/Cip1, despite ecient inhibition of 1994; Toyoshima and Hunter, 1994; Lee et al., 1995; cyclin E, A and B1 dependent kinase activity, suggesting Matsuoka et al., 1995). -
ATR Pathway Inhibition Is Synthetically Lethal in Cancer Cells with ERCC1 Deficiency
Published OnlineFirst March 24, 2014; DOI: 10.1158/0008-5472.CAN-13-3229 Cancer Therapeutics, Targets, and Chemical Biology Research ATR Pathway Inhibition Is Synthetically Lethal in Cancer Cells with ERCC1 Deficiency Kareem N. Mohni, Gina M. Kavanaugh, and David Cortez Abstract The DNA damage response kinase ATR and its effector kinase CHEK1 are required for cancer cells to survive oncogene-induced replication stress. ATR inhibitors exhibit synthetic lethal interactions, with deficiencies in the DNA damage response enzymes ATM and XRCC1 and with overexpression of the cell cycle kinase cyclin E. Here, we report a systematic screen to identify synthetic lethal interactions with ATR pathway–targeted drugs, rationalized by their predicted therapeutic utility in the oncology clinic. We found that reduced function in the ATR pathway itself provided the strongest synthetic lethal interaction. In addition, we found that loss of the structure-specific endonuclease ERCC1-XPF (ERCC4) is synthetic lethal with ATR pathway inhibitors. ERCC1- deficient cells exhibited elevated levels of DNA damage, which was increased further by ATR inhibition. When treated with ATR or CHEK1 inhibitors, ERCC1-deficient cells were arrested in S-phase and failed to complete cell-cycle transit even after drug removal. Notably, triple-negative breast cancer cells and non–small cell lung cancer cells depleted of ERCC1 exhibited increased sensitivity to ATR pathway–targeted drugs. Overall, we concluded that ATR pathway–targeted drugs may offer particular utility in cancers with reduced ATR pathway function or reduced levels of ERCC4 activity. Cancer Res; 74(10); 1–11. Ó2014 AACR. Introduction repair pathway such as homologous recombination or post- – Replicating DNA is sensitive to a wide array of endogenous replicative repair to remove the PARP DNA complexes (7). -
Cyclin-Dependent Kinase Inhibitors KRP1 and KRP2 Are Involved in Grain Filling and Seed Germination in Rice (Oryza Sativa L.)
International Journal of Molecular Sciences Article Cyclin-Dependent Kinase Inhibitors KRP1 and KRP2 Are Involved in Grain Filling and Seed Germination in Rice (Oryza sativa L.) Abolore Adijat Ajadi 1,2, Xiaohong Tong 1, Huimei Wang 1, Juan Zhao 1, Liqun Tang 1, Zhiyong Li 1, Xixi Liu 1, Yazhou Shu 1, Shufan Li 1, Shuang Wang 1,3, Wanning Liu 1, Sani Muhammad Tajo 1, Jian Zhang 1,* and Yifeng Wang 1,* 1 State Key Lab of Rice Biology, China National Rice Research Institute, Hangzhou 311400, China; [email protected] (A.A.A.); [email protected] (X.T.); [email protected] (H.W.); [email protected] (J.Z.); [email protected] (L.T.); [email protected] (Z.L.); [email protected] (X.L.); [email protected] (Y.S.); [email protected] (S.L.); [email protected] (S.W.); [email protected] (W.L.); [email protected] (S.M.T.) 2 Biotechnology Unit, National Cereals Research Institute, Badeggi, Bida 912101, Nigeria 3 College of Life Science, Yangtze University, Jingzhou 434025, China * Correspondence: [email protected] (J.Z.); [email protected] (Y.W.); Tel./Fax: +86-571-6337-0277 (J.Z.); +86-571-6337-0206 (Y.W.) Received: 21 November 2019; Accepted: 26 December 2019; Published: 30 December 2019 Abstract: Cyclin-dependent kinase inhibitors known as KRPs (kip-related proteins) control the progression of plant cell cycles and modulate various plant developmental processes. However, the function of KRPs in rice remains largely unknown. In this study, two rice KRPs members, KRP1 and KRP2, were found to be predominantly expressed in developing seeds and were significantly induced by exogenous abscisic acid (ABA) and Brassinosteroid (BR) applications. -
Involvement in Endoreduplication (Cell Cycle/Repa/Wheat Dwarf Virus) GIDEON GRAFI*T#, RONALD J
Proc. Natl. Acad. Sci. USA Vol. 93, pp. 8962-8967, August 1996 Cell Biology A maize cDNA encoding a member of the retinoblastoma protein family: Involvement in endoreduplication (cell cycle/RepA/wheat dwarf virus) GIDEON GRAFI*t#, RONALD J. BURNETTr*, TIM HELENTJARIS*, BRIAN A. LARKINS*§, JAMES A. DECAPRIOt, WILLIAM R. SELLERSt, AND WILLIAM G. KAELIN, JR.t *Department of Plant Sciences, University of Arizona, Tucson AZ 85721; and tDana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115 Contributed by Brian A. Larkins, May 14, 1996 ABSTRACT Retinoblastoma (RB-1) is a tumor suppres- We identified a partial maize cDNA (ZmRB) that is pre- sor gene that encodes a 105-kDa nuclear phosphoprotein. To dicted to encode a protein with homology to members of the date, RB genes have been isolated only from metazoans. We pocket protein (Rb) family. Here we provide evidence that have isolated a cDNA from maize endosperm whose predicted ZmRb is a member of the retinoblastoma protein family and protein product (ZmRb) shows homology to the "pocket" A demonstrate its ability to bind the replication-associated pro- and B domains of the Rb protein family. We found ZmRb tein WDV RepA and its involvement in the process of DNA behaves as a pocket protein based on its ability to specifically endoreduplication during maize endosperm development. interact with oncoproteins encoded by DNA tumor viruses (E7, T-Ag, E1A). ZmRb can interact in vitro and in vivo with MATERIALS AND METHODS the replication-associated protein, RepA, encoded by the wheat dwarf virus. The maize Rb-related protein undergoes Plant Materials and Chemicals. -
Supplementary Table S1. Correlation Between the Mutant P53-Interacting Partners and PTTG3P, PTTG1 and PTTG2, Based on Data from Starbase V3.0 Database
Supplementary Table S1. Correlation between the mutant p53-interacting partners and PTTG3P, PTTG1 and PTTG2, based on data from StarBase v3.0 database. PTTG3P PTTG1 PTTG2 Gene ID Coefficient-R p-value Coefficient-R p-value Coefficient-R p-value NF-YA ENSG00000001167 −0.077 8.59e-2 −0.210 2.09e-6 −0.122 6.23e-3 NF-YB ENSG00000120837 0.176 7.12e-5 0.227 2.82e-7 0.094 3.59e-2 NF-YC ENSG00000066136 0.124 5.45e-3 0.124 5.40e-3 0.051 2.51e-1 Sp1 ENSG00000185591 −0.014 7.50e-1 −0.201 5.82e-6 −0.072 1.07e-1 Ets-1 ENSG00000134954 −0.096 3.14e-2 −0.257 4.83e-9 0.034 4.46e-1 VDR ENSG00000111424 −0.091 4.10e-2 −0.216 1.03e-6 0.014 7.48e-1 SREBP-2 ENSG00000198911 −0.064 1.53e-1 −0.147 9.27e-4 −0.073 1.01e-1 TopBP1 ENSG00000163781 0.067 1.36e-1 0.051 2.57e-1 −0.020 6.57e-1 Pin1 ENSG00000127445 0.250 1.40e-8 0.571 9.56e-45 0.187 2.52e-5 MRE11 ENSG00000020922 0.063 1.56e-1 −0.007 8.81e-1 −0.024 5.93e-1 PML ENSG00000140464 0.072 1.05e-1 0.217 9.36e-7 0.166 1.85e-4 p63 ENSG00000073282 −0.120 7.04e-3 −0.283 1.08e-10 −0.198 7.71e-6 p73 ENSG00000078900 0.104 2.03e-2 0.258 4.67e-9 0.097 3.02e-2 Supplementary Table S2. -
Signature of Progression and Negative Outcome in Colorectal Cancer
Oncogene (2010) 29, 876–887 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 $32.00 www.nature.com/onc ORIGINAL ARTICLE A ‘DNA replication’ signature of progression and negative outcome in colorectal cancer M-J Pillaire1,7, J Selves2,7, K Gordien2, P-A Gouraud3, C Gentil3, M Danjoux2,CDo3, V Negre4, A Bieth1, R Guimbaud2, D Trouche5, P Pasero6,MMe´chali6, J-S Hoffmann1 and C Cazaux1 1Genetic Instability and Cancer Group, Department Biology of Cancer, Institute of Pharmacology and Structural Biology, UMR5089 CNRS, University of Toulouse, University Paul Sabatier, Toulouse, France; 2INSERM U563, Federation of Digestive Cancerology and Department of Anatomo-pathology, University of Toulouse, University Paul Sabatier, Toulouse, France; 3Service of Epidemiology, INSERM U558, Faculty of Medicine, University of Toulouse, University Paul Sabatier, Alle´es Jules Guesde, Toulouse, France; 4aCGH GSO Canceropole Platform, INSERM U868, Val d’Aurelle, Montpellier, France; 5Laboratory of Cellular and Molecular Biology of Cell Proliferation Control, UMR 5099 CNRS, University of Toulouse, University Paul Sabatier, Toulouse, France and 6Institute of Human Genetics UPR1142 CNRS, Montpellier, France Colorectal cancer is one of the most frequent cancers Introduction worldwide. As the tumor-node-metastasis (TNM) staging classification does not allow to predict the survival of DNA replication in normal cells is regulated by an patients in many cases, additional prognostic factors are ‘origin licensing’ mechanism that ensures that it occurs needed to better forecast their outcome. Genes involved in just once per cycle. Once cells enter the S-phase, the DNA replication may represent an underexplored source stability of DNA replication forks must be preserved to of such prognostic markers. -
Perspectives
CopyTight 0 1997 by the Genetics Society of America Perspectives Anecdotal, Historical And Critical Commentaries on Genetics Edited by James F. Crow and William F. Dove Chromosome Changes in Cell Differentiation Orlando J. Miller Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan 48201 N a recent “Perspectives” article, EEVA THEW the H19 gene. The maternal H19 allele is expressed, I (1995) called attention to a variety of alterations and its cis-acting, nontranslatable RNA product inhibits in chromosomes that occur regularly in differentiating the expression of the maternal alleles of the other three cells, have been known for many years, and are still genes, mash-2, Ins-2, and I@. The paternal H19 allele poorly understood. Theseincludedfacultatiue heterochro- is methylated and notexpressed, so the paternal alleles matinization, polyploidization by endoreduplication, under- of the other three genes are expressed. Imprinting of replication ofsome sequences inpolytene chromosomes, the Inns-2 and I@ genes is disrupted by maternal inheri- and gene amplijication. The related programmed DNA tance of a targeted deletion of the H19 gene and its loss phenomena called chromatin diminutionand chromo- flanking sequence, while paternal inheritance has no some eliminationalso belong tothis group of highly regu- effect, reflecting the normally silent state of the pater- lated developmental chromosomechanges. Here Ishall nal HI 9 allele (LEIGHTONet al. 1995). There is also a briefly review these changes, with particular emphasis cluster of several genes on human chromosome 15 that on thecell and molecular genetic approaches thathave are expressed exclusively on thepaternal chromosome; provided, or could provide, insights into the signaling these may play a role in thePrader-Willi syndrome. -
Endoreduplication in Drosophila Melanogaster Progeny After Exposure to Acute Γ-Irradiation
bioRxiv preprint doi: https://doi.org/10.1101/376145; this version posted July 24, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Endoreduplication in Drosophila melanogaster progeny after exposure to acute γ-irradiation Running head: Endoreduplication in Drosophila after γ- Keywords: giant chromosomes, polyteny degree, developmental rate, embryonic mortality, ionizing radiation. Daria A. Skorobagatko VN Karazin Kharkiv National University, Department of Genetics and Cytology, Svobody sq., 4, Kharkiv, 61022, Ukraine E-mail: [email protected] Phone: +380673007826 Alexey A. Mazilov Ph D NSC ‘Kharkiv Institute of Physics and Technology’, Department of Physics of Radiation and Multichannel Track Detectors, Academic str., 1, Kharkiv, 61108, Ukraine E-mail: [email protected] Phone: +380679950495 Volodymyr Yu. Strashnyuk Dr Sci (corresponding author) VN Karazin Kharkiv National University, Department of Genetics and Cytology, Svobody sq., 4, Kharkiv, 61022, Ukraine E-mail: [email protected] Phone: +380679478350 bioRxiv preprint doi: https://doi.org/10.1101/376145; this version posted July 24, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 2 Abstract The purpose of investigation was to study the effect of acute γ-irradiation of parent adults on the endoreduplication in Drosophila melanogaster progeny. As a material used Oregon-R strain. Virgin females and males of Drosophila adults at the age of 3 days were exposed at the doses of 8, 16 and 25 Gy. Giant chromosomes were studied at late 3rd instar larvae by cytomorphometric method. -
A Review of Prostate Cancer Genome-Wide Association Studies (GWAS)
Published OnlineFirst January 18, 2018; DOI: 10.1158/1055-9965.EPI-16-1046 Review Cancer Epidemiology, Biomarkers A Review of Prostate Cancer Genome-Wide & Prevention Association Studies (GWAS) Sarah Benafif1, Zsofia Kote-Jarai1, and Rosalind A. Eeles1,2, on behalf of the PRACTICAL Consortium Abstract Prostate cancer is the most common cancer in men in for population-based risk stratification to target prostate Europe and the United States. The genetic heritability of cancer screening to men with an increased genetic risk of prostate cancer is contributed to by both rarely occurring disease development, while for those who develop prostate genetic variants with higher penetrance and moderate cancer, identifying genetic variants could allow treatment to commonly occurring variants conferring lower risks. to be tailored based on a genetic profile in the early disease The number of identified variants belonging to the latter setting. Functional studies of identified variants are needed category has increased dramatically in the last 10 years with to fully understand underlying mechanisms of disease the development of the genome-wide association study and identify novel targets for treatment. This review will (GWAS) and the collaboration of international consortia outline the GWAS carried out in prostate cancer and the that have led to the sharing of large-scale genotyping data. common variants identified so far, and how these may be Over 40 prostate cancer GWAS have been reported, with utilized clinically in the screening for and management of approximately 170 common variants now identified. prostate cancer. Cancer Epidemiol Biomarkers Prev; 27(8); 845–57. Clinical utility of these variants could include strategies Ó2018 AACR. -
Endoreduplication in Floral Structure, Vegetative and Fruits of Red Pitaya with White Pulp
931 Original Article ENDOREDUPLICATION IN FLORAL STRUCTURE, VEGETATIVE AND FRUITS OF RED PITAYA WITH WHITE PULP ENDORREDUPLICAÇÃO EM ESTRUTURA FLORAL, VEGETATIVA E FRUTOS DE PITAYA VERMELHA DE POLPA BRANCA Thatiane Padilha de MENEZES 1; Leila Aparecida Salles PIO 2; José Darlan RAMOS 3; Moacir PASQUAL 4; Tesfahum Alemu SETOTAW5 1. Doutora em Agronomia, Universidade Federal de Lavras – UFLA, Lavras, MG, Brasil. [email protected]; 2. Professora, Doutora em Agronomia, Universidade Federal de Lavras – UFLA, Lavras, MG, Brasil; 3. Professor, Doutor em Agronomia, Universidade Federal de Lavras – UFLA, Lavras, MG, Brasil; 4. Professor, Doutor em Agronomia, Universidade Federal de Lavras – UFLA, Lavras, MG, Brasil. [email protected]; 5. Doutor em Agonomia, Universidade Federal de Lavras – UFLA, Lavras, MG, Brasil. ABSTRACT: Endoreduplication is the change of cellular cycle that result DNA duplication without cell division and could result endopolyploid cells. This phenomenon is common in plants and animals and considered as evaluative strategy. Although endoreduplication reported in various plant species, the information about these phenomena in red pitaya is rare. Therefore, this work was done with the objective of studying the endoreduplication in Hylocereus undatus Haw. using flow cytometry analysis. In this study were used the tissue from the flower structure, fruits, roots, cladode, and thorns of the pitaya plant.To determine the DNA content approximately 50 mg the sample of each treatment with Pisum sativum (the internal standard reference) were grind in plate of petri dishes contained 1 mL of cold Marie buffer to release the nucleus.The nuclear suspension was filtered through 50 µm mesh. The nucleuses were colored with 25 µL of 1 mg/L mL of propidium iodide. -
SAMBA, a Plant-Specific Anaphase-Promoting Complex/Cyclosome Regulator Is Involved in Early Development and A-Type Cyclin Stabilization Nubia B
SAMBA, a plant-specific anaphase-promoting complex/cyclosome regulator is involved in early development and A-type cyclin stabilization Nubia B. Eloy, Nathalie Gonzalez, Jelle van Leene, Katrien Maleux, Hannes Vanhaeren, Liesbeth de Milde, Stijn Dhondt, Leen Vercruysse, Erwin Witters, Raphaël Mercier, et al. To cite this version: Nubia B. Eloy, Nathalie Gonzalez, Jelle van Leene, Katrien Maleux, Hannes Vanhaeren, et al.. SAMBA, a plant-specific anaphase-promoting complex/cyclosome regulator is involved in early de- velopment and A-type cyclin stabilization. Proceedings of the National Academy of Sciences of the United States of America , National Academy of Sciences, 2012, 109 (34), pp.13853 - 13858. 10.1073/pnas.1211418109. hal-01190736 HAL Id: hal-01190736 https://hal.archives-ouvertes.fr/hal-01190736 Submitted on 29 May 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. SAMBA, a plant-specific anaphase-promoting complex/ cyclosome regulator is involved in early development and A-type cyclin stabilization Nubia B. Eloya,b, Nathalie Gonzaleza,b, Jelle Van Leenea,b, Katrien Maleuxa,b, Hannes Vanhaerena,b, Liesbeth De Mildea,b, Stijn Dhondta,b, Leen Vercruyssea,b, Erwin Wittersc,d,e, Raphaël Mercierf, Laurence Cromerf, Gerrit T.