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Progress in Cell Cycle Research Volume 4 A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher. Progress in Cell Cycle Research Volume 4 Edited by Laurent Meijer Armelle Jezequel Centre National de la Recherche Scientifique Roscoff, France and Bernard Ducommun Universite Paul Sabotier Centre National de la Recherche Scientifique Toulouse, France SPRINGER SCIENCE+BUSINESS MEDIA, LLC Front cover. PTK1 cells after cytokinesis (micrograph courtesy of Dr. Conly L. Rieder) ISSN 1087-2957 ISBN 978-1-4613-6909-7 ISBN 978-1-4615-4253-7 (eBook) DOI 10.1007/978-1-4615-4253-7 © 2000 Springer Science+Business Media New York Originally published by Kluwer Academic / Plenum Publishers in 2000 Softcover reprint of the hardcover 1st edition 2000 http://www.wkap.nl/ 10 9 8 7 6 5 4 3 21 All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher Preface The "Progress in Cell Cycle Research" series is dedicated to serve as a collection of reviews on various aspects of the cell division cycle, with special emphasis on less studied aspects. We hope this series will continue to be helpful to students, graduates and researchers interested in the cell cycle area and related fields. We hope that reading of these chapters will constitute a "point of entry" into specific aspects of this vast and fast moving field of research. As PCCR4 is being printed several other books on the cell cycle have appeared (ref. 1-3) which should complement our series. This fourth volume of PCCR starts with a review on RAS pathways and how they impinge on the cell cycle (chapter 1). In chapter 2, an overview is presented on the links between cell anchorage -cytoskeleton and cell cycle progression. A model of the Gl control in mammalian cells is provided in chapter 3. The role of histone acetylation and cell cycle contriol is described in chapter 4. Then follow a few reviews dedicated to specific cell cycle regulators: the 14-3-3 protein (chapter 5), the cdc7/Dbf4 protein kinase (chapter 6), the two products of the pI6/CDKN2A locus and their link with Rb and p53 (chapter 7), the Ph085 cyclin-dependent kinases in yeast (chapter 9), the cdc25 phophatase (chapter 10), RCCI and ran (chapter 13). The intriguing phosphorylation dependent prolyl-isomerization process and its function in cell cycle regulation are reviewed in chapter 8. Our current knowledge of the molecular mechanisms of cell cycle regulation has greatly benefited from the use of oocyte maturation, a unique but diverse cellular process investigated in a large variety of models reviewed in chapter 11. The cross-talks between MAP kinase and cdc2/ cyclin B in oocytes have been particularly well understood in Xenopus (Chapter 12). More and more data show the interference of viral proteins with the mammalian cell cycle (see review in chapter 1 of PCCR3 I). One such example, the HfLV-I tax protein, is described in chapter 14. Our knowledge of the cell cycle is spreading to protozoan parasites, as nicely reviewed in chapter 15, and this may have great therapeutical consequences. Quite fascinatingly, the cell cycle is regulated by the circadian rhythm, from unicellular organisms (chapter 16) to man (chapter 17). The use of cell cycle specific treatments in cancer therapy may greatly benefit from understanding and use of the links between the cycle and the rhythm. Major advances have been recently made in the identification of the molecular actors regulating the circadian rhythm. We anticipate that some cell cycle and circadian rhythm regulators will soon be found to be connected! The treatment of cancer (and other cell cycle related diseases) will also obviously benefit from a better understanding of the connections between cell cycle and apoptosis (chapter 18). As more and more "cell cycle drugs" are being discovered, their use as anticancer drugs is being extensively investigated; they are reviewed in chapter 19. The discovery of cell cycle regulators in the brain of Alzheimer's disease patients, leaves us with the idea that cell cycle studies, initially supported by the antitumour purpose, may have applications in quite unexpected fields. We are particularly grateful to the contributors of PCCR4 who have accepted to spend a bit of their time away from the bench and their mainstream articles to write a review on their field of interest. We also thank the members of the Roscoff Cell Cycle Group for help and support and acknowledge the efficiency of the editorial staff at Plenum Press. The support of the C.N.RS. ("Centre National de la Recherche Scientifique") and the "Conseil Regional de Bretagne" is also to be acknowledged. Roscoff, Bretagne, France Laurent MEIJER Armelle JEZEQUEL Bernard DUCOMMUN 1. Ruffolo, RR, Poste, G. & Metcalf, B.W. (editors), (1997). Cel cycle regulation. Harwood Academic Publishers, 174pp. 2. Francis, D., Dudits, D. & fuze, D. (editors) (1998). Plant Cell Division. Portland Press, London & Miami, Research Monograph X, 347 pp. 3. Stein, G.S., Baserga, R., Giordano, A. and Denhardt, D.T. (editors), (1999) The molecular basis of cell cycle and growth control. Wiley-Liss, New York, 389 pp. v Contents Relationship between RAS pathways and cell cycle control Mlrk E. Ewen 1 Cell-anchorage, cell cytoskeleton, and Rho-GTPase family in regulation of cell cycle progression Ichiro Tatsuno, Aizan Hirai, and Yaushi Saito 19 The Continuum model and G1-control of the mammalian cell cycle Stephen Cooper 27 Histone acetylation and the control of the cell cycle Laura Magnaghi-Jaulin, Slimane Ait-Si-Ali, and Annick Harel-Bellan 41 14-3-3 proteins and growth control Wronique Baldin 49 A Cdc7p-Dbf4 protein kinase activity is conserved from yeast to humans Leland H. Johnston, Hisao MJisai, and Akio Sugino 61 Alternative product of the pl6/CKDN2A locus connects the Rb and p53 tumor suppressors Marion C. James, and Gordon Peters 71 Phosphorylation-dependent prolyl isomerization: a novel cell cycle regulatory mechanism KunPing Lu 83 Functions of Pho85 cyclin-dependent kinases in budding yeast Jason Moffat, Dongqing Huang, and Brenda Andrews 97 Cell cycle regulation by the Cdc25 phosphatase family Ida Nilsson, and Ingrid Hoffmann 107 Molecular mechanisms of the initiation of oocyte maturation: general and species-specific aspects Mlsakane Yamashita, Koichi Mita, Noriyuki Yoshida, and Tomoko Kondo 115 The activation of MAP kinase and p34cdc2/cyclin B during the meiotic maturation of Xenopus oocytes Amparo Palmer and Angel R. Nel:treda 131 Premature chromatin condensation caused by loss of RCa Hitoshi Nishijima, Takashi Seki, Hideo Nishitani, and Takeharu Nishimoto 145 HTL V- I tax and cell cycle progression Christine Neuveut, and Kuan-Teh Jeang 157 The cell cycle in protozoan parasites Christian Doerig, Debopam Chakrabarti, Barbara Kappes, and Keith Matthews 163 Circadian control of cell division in unicellular organisms Tetsuya Mori, and Carl H. Johnson 185 Circadian variation of cell proliferation and cell cycle protein expression in man: clinical implications Georg Bjarnason, and Richard Jordan 193 VII Molecular switches that govern the balance between proliferation and apoptosis Bert Schutte, and Frans C.S. Ramaekers 207 Molecular events that regulate cell proliferation: an approach for the development of new anticancer drugs Eve Damiens 219 Abortive oncogeny and cell cycle-mediated events in Alzheimer disease Arun K. Raina, Xiongwei Zhu, Mervyn Monteiro, Atsushi Takeda, and Mark A. Smith 235 Contributors 243 Index 245 VIII Progress in Cell Cycle Research, Vol. 4, 1-17, (2000) (Meijer, L., Jezequel, A., and Ducommun, B., eds.) Kluwer Academic /Plenum Publishers, New York chapter 1 Relationship between Ras pathways and cell cycle control MarkE.Ewen Dana-Farber Cancer Institute, Harvard Medical School 44 Binney Street, Boston, MA 02115, USA. The ordered execution of the two main events of cellular reproduction, duplication of the genome and cell division, characterize progression through the cell cycle. Cultured cells can be switched between cycling and non-cycling states by alteration of extracellular conditions and the notion that a critical cellular control mechanism presides on this decision, whose temporal loCation is known as the restriction point, has become the focus for the study of how extracellular mitogenic signalling impinges upon the cell cycle to influence proliferation. This review attempts to cover the disparate pathways of Ras-mediated mitogenic signal transduction that impact upon restriction point control. MITOGENIC SIGNALLING AND THE Gl cells it must not only duplicate its genetic material PHASE OF THE CELL CYCLE but must also double its total biomass. This simple analysis suggests there exists some measure of co The ordered execution of the two main events of ordination between control of both the chromosomal cellular reproduction, duplication of the genome and (DNA) cycle and cellular protein biosynthesis. In cell division, characterize progression through the support of this notion, cells treated in Gl prior to the mammalian cell cycle. These two readily discernible R point with doses of cycloheximide sufficient to processes, DNA synthesis (S phase) and mitosis (M cause a moderate inhibition of protein synthesis also phase), and the "gaps" between them, G1 (before S) arrest with a G1 DNA content, while those treated and G2 (before M) thus provide an operational after R, or in S, G2 or M continue to execute the cell subdivision of the cell cycle into four discrete phases. cycle program to become arrested in the following Cells can exist in an alternative "out of cycle" state (of G1(4, 7-9). Indeed, Pardee's original definition of the minimal metabolism) known as quiescence R point was made upon sensitivity to cycloheximide (designated GO), and the rate of proliferation in a as well as dependency on serum factors. given population (of cells) is largely determined by the relative proportions of cycling versus quiescent Taken together, these observations indicate that cells. both sufficient biosynthetic capacity and appropriate extracellular signals are required for passage through Cells in culture can be switched between the R point and initiation of a new round of cellular proliferative (cycling) and quiescent (non-cycling) replication. The bigger question of whether states by alteration of extracellular conditions (e.g. mitogenic signalling pathways impacts simulta nutrient availability, mitogen concentration) and the neously yet independently upon the processes of notion that a critical cellular control mechanism biosynthesis and the chromosome cycle, or whether presides over this decision, whose temporal location the stimulation of one results in the co-ordinate is known as the restriction point, has become the regulation of the other (as a fait a compli) remains to focus for the study of how extracellular mitogenic be answered. In any case, what is clear is that R is a signalling impinges upon the cell cycle to influence common point of convergence. In the following proliferation. pages, I will attempt to review the disparate Quiescent cells have a 2N DNA content, the same pathways of Ras-mediated mitogenic signal trans as those in G1, suggesting that the switch to and from duction that impact upon restriction point control. GO is made during this phase. Indeed, seminal observations made nearly twenty-five years ago by THE DISCOVERY OF RAS Pardee showed that there is a window of time in G1 Concurrent with the development of the notion of during which serum factors are absolutely required the restriction point, a seemingly unrelated field of for further progress into the remainder of the cycle investigation led to the discovery of a class of genes (1). It is the point at which the cell loses its involved in cellular transformation known as dependency upon extracellular conditions for cell oncogenes. Many of these gene products would cycle progression that he defined as R (reviewed in eventually be shown to participate in mitogenic (2-5) ). In murine fibroblasts R lies about two hours signalling during GO and G1. prior to the initiation of S phase. Similar work in chicken cells also suggested that R lies somewhere in Virology has long provided important cues in the mid to late Gl(6). Additionally, it is self evident that study of mammalian cells. It was an understanding of the transforming potential of RNA tumor viruses before a cell can divide to produce two daughter 1 M.E.EWEN (in particular retroviruses) at the molecular level that (proto-oncogene), is due to a single point mutation in paved the way to the discovery of oncogenes. Work its coding sequence (27-29). Similarly, retroviruses some thirty years ago on an avian RNA virus called harbouring the ras oncogene also encode a mutant Rous sarcoma virus (10) provided an understanding oncogenic form of the protein. Since the discovery of of how a virally encoded "transforming potential" ras over 30 oncogenes have been identified, of which, could be propagated genetically (11-13). Further ras is the most frequently mutated in human cancer more, these investigations provided the molecular (30). tools to ask about the nature of this "transforming LINKING RAS TO Gl PROGRESSION potential". AND RESTRICTION POINT CONTROL A key to the answer was the observation that the Ras biochemistry: active and inactive forms transforming avian sarcoma viruses contained more The manner of its discovery-as an oncogene that genetic information than their nontransforming provides a selective advantage to tumor cells: counterparts. Both types of viruses were equally suggested that Ras might have some role ~ competent in their ability to infect cells and replicate proliferation or growth control. Though this and it was therefore assumed that the additional assumption is for the most part correct, it is rather genetic information carried by the transforming naive given what we now know of other cellular viruses was not involved in viral replication per se processes, principally cell adhesion and cell death but rather in providing the virus with a selective mechanisms, whose derangement's provide tumor growth advantage. Utilising both strains of Rous cells with a growth advantage. Keys to sarcoma virus, Bishop, Varmus and co-workers understanding the cellular functions of Ras were the isolated the extra genetic material carried by the discoveries that this 21 kilodalton protein possesses transforming virus, which they termed cDNA sarc guanine nucleotide binding activity and has intrinsic for cDNA-bearing sarcoma producing gene GTPase activity (31-33). Oncogenic mutants of Ras sequences, now commonly referred to as v-Src, as the were shown to either exhibit decreased GTPase first, and prototypic, oncogene (14). activity or to increase the rate of exchange of bound Surprisingly, when the v-Src cDNA was used as a GDP for free GTP. Within the cell the concentration probe, it was found to be present in the genomes of of GTP is ten times that of GDP. It was thus correctly nontransformed avian cells (15) as well as in cells assumed that GTP-bound Ras was the active form from several other species, including humans. The and the GDP-bound form was inactive. significance of this observation was that it would Linking Ras to the action of growth factor and subsequently become clear that cellular genes, with cytokine receptors normal functions, comprised the transforming It was found that oncogenic and wild type Ras potential of many retroviruses. Using a similar were post-translationally modified via covalent methodology, Scolnick and colleagues isolated the attachment of lipid which anchored the protein to ras (from rat sarcoma) genes, Ha-ras and Ki-ras (16), the inner plasma membrane (34-36) . This placed Ras as the transforming genes of the Harvey and Kirsten in the proximity of membrane receptors involved in strains of rat sarcoma viruses (17, 18), respectively. extracellular signalling. The importance of these Both of these viral genes were also shown to be observations came to light in 1990 when the first present in the genomes of several species including humans (19). Later a distinction was made, and the physiological stimulus controlling Ras activation was identified. Activation of the T cell receptor (TCR) or normal cellular homologues of viral oncogenes were referred to as proto-oncogenes. the interleukin 2 receptor causes a rapid stimulation of Ras, as measured by the ratio of GTP- to GDP In the early 80s ras genes were discovered by a bound forms of the protein coincident with the completely independent route. Several laboratories induction of cell proliferation (37). TCR initiates the had shown that DNA fragments from animal and GOjGl transition and interleukin 2 receptor the human tumors or chemically transformed cells could GljS transition, suggesting that Ras regulates transform the "normal" mouse NIH 3T3 fibroblasts progression through Gl via multiple receptors. line (20-22). Such experiments were motivated by Similar observations were made in murine studies on bacterial virulence performed four fibroblasts with respect to the effects of PDGF, EGF decades earlier by Avery that led to the seminal and insulin in promoting progression from GO to Gl demonstration that DNA was the genetic material and Gl to S phase (9, 38). Various growth factors (23). have been defined by virtue of their ability to In this way, the laboratories of Weinberg, Cooper facilitate the GOjGl transition, initiated a process and Wigler identified ras as one of the genes isolated called competence, and the GljS transition, from human cancer lines capable of transforming involving progression through the restriction point rodent cells in culture (24-26). The ability of ras to (3). We now know that activation of several growth cause oncogenic transformation, in contrast to its factor and cytokine receptors stimulate the activity of non-transforming wild type cellular homologue Ras. Together, these studies circumstantially 2 CHAPTER 1/ RAS AND TIlE CELL CYCLE receptor tyrosine kinase cell membrane • COP-bound inactive Ras I fa~r-mediatecl growth • receptor activation receptor phosphorylati(ln and activation CIT-bound active Ras SH2-mediated interaction SI-I3-mediated interaction Figure 1. Growth factor stimulation leads to receptor tyrosine kinase activation and autoph08phorylation. Phosphorylation of the receptor provides a docking site for cytosolic Grb2-Sos complexes, resulting in the recruitment of this complex to the plasma membrane, where Ras is anchored. Recruitment of Sos to the membrane allows it to promote the exchange of GOP for GIT on Ras, resulting in its activation. link the action of extracellular factors that influence function of the particular cell type used. the progression from GO to S phase, various Alternatively, they can be explained by differing membrane receptors, and the activation of Ras. degrees of the absolute amount of activated Ras achieved in each experimental system, although Ras and the cell cycle these irregularities may equally reflect additional More direct experiments addressed the complexities. importance of Ras in cell cycle control. Microinjection of activated or wild type Ras was UPSTREAM AND DOWNSTREAM OF RAS found to induce DNA synthesis from quiescence (39, 40), suggesting that Ras is sufficient for progreSSion Ras functions ultimately as a signal transducer. In from GO to S phase. In addition, experiments order to understand how Ras affects cell cycle involving microinjection of a Ras neutralising progression it is therefore important to know how antibody or expression of a dominant-negative Ras is activated, and once active, how it transmits mutant of Ras have demonstrated that Ras is signals. Below I summarise how receptor activation required for progression from GO to a point in late leads to the stimulation of Ras activity and the G1, roughly coinciding with the restriction point (41- downstream effector pathways in which Ras 44). signalling operates. However, it is noteworthy that depending on the How receptor tyrosine kinases activate Ras particular cellular system and the experimental It took nearly ten years from its discovery to approach used, there is some variation on the results begin to elucidate how various growth factors and described above. For example, using an inducible cytokines regulate the activity of Ras (Figure 1). system, expression of one of the oncogenic forms of Signalling is initiated by growth factors binding to Ras, Ras(V12), was insufficient to induce S phase their receptors, which in tum induce receptor entry from a serum-starved state (45). Lilcewise, "add dimerization and trans tyrosine phosphorylation back" experiments using mutant PDGF receptors (autophosphorylation). These phosphotyrosine capable of discriminately activating various signal residues, in a particular context, are recognised by transduction pathways suggested that activation of the adaptor molecule, Grb2, through its SID domain Ras alone was not sufficient to induce DNA synthesis (Src homology domain 2). Grb2 associates with 50s, a (46). These apparent discrepancies lilcely reflect the nucleotide exchange factor for Ras. The interaction difference in the mitogenic potential of Ras as a between Grb2 and 50s is mediated via two SH3 3

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