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• W2009780792 abstract "Single-celled organisms monitor cell geometry and use this information to control cell division. Such geometry-sensing mechanisms control both the decision to enter into cell division and the physical orientation of the chromosome segregation machinery, suggesting that signals controlling cell division may be linked to the mechanisms that ensure proper chromosome segregation. Single-celled organisms monitor cell geometry and use this information to control cell division. Such geometry-sensing mechanisms control both the decision to enter into cell division and the physical orientation of the chromosome segregation machinery, suggesting that signals controlling cell division may be linked to the mechanisms that ensure proper chromosome segregation. How cells coordinate growth and division is an important problem for cell and developmental biology. Cell size and shape impact the cell division process because chromosomes and other cellular components must be properly segregated within a confined space. As cells grow and progress toward division, a series of checkpoints ensure that cells do not prematurely undergo cell-cycle transitions such as entry into S phase or mitosis. Cell-cycle studies have revealed the existence of cell size checkpoints that link cell-cycle transitions with the attainment of critical cell size thresholds. These observations raise a number of questions, including “what is size?” and “how is size measured?” Work in a number of single-celled organisms has led to the idea that cell geometry may have a role in the assessment of size and how size relates to the cell-cycle checkpoints that operate during chromosome segregation and division. In this Essay, we examine the evidence and emerging themes that surround geometry-sensing mechanisms in two well-studied model systems: bacteria and yeast. We suggest that the role of geometry in controlling cell-cycle decisions at division may be linked to the role of cell geometry in physically guiding chromosome segregation in these organisms. This raises the possibility that cell-cycle controls over entry into mitosis may be linked to the mechanisms that ensure proper execution of mitosis and cytokinesis. Connections between cell geometry and cell division have been well described in several bacterial species, providing a good framework for understanding the general design principles of geometry-sensing mechanisms. In these bacterial cells, division occurs in the cell middle due to locally restricted assembly of the cytokinetic Z-ring composed of tubulin-like FtsZ. Two mechanisms prevent Z-ring assembly at the cell ends, thus incorporating geometric information into the division process. The first is in the bacterium Escherichia coli and uses a self-organized oscillator comprised of the MinCDE proteins. The second mechanism requires a self-assembled filament network that senses membrane curvature and is found in both Bacillus subtilis and Caulobacter crescentus. These two systems both inhibit division at the cell ends and demonstrate that mechanisms based on quite different molecular components can integrate geometric information with cell division. The MinCDE system is a remarkable geometry-measuring oscillator, the mechanism of which has been elucidated using a combination of elegant experimental and computational approaches. In this three-component system, MinC inhibits the assembly of tubulin-like FtsZ, MinD recruits MinC to the cell membrane, and MinE controls intracellular organization of MinCD (for reviews see Lutkenhaus, 2007Lutkenhaus J. Annu. Rev. Biochem. 2007; 76: 539-562Crossref PubMed Scopus (429) Google Scholar, Lutkenhaus, 2008Lutkenhaus J. Adv. Exp. Med. Biol. 2008; 641: 49-61Crossref PubMed Scopus (24) Google Scholar). The interaction of MinD and MinE generates oscillatory behavior in which MinCD migrates back and forth between the two cell poles (Raskin and de Boer, 1997Raskin D.M. de Boer P.A. Cell. 1997; 91: 685-694Abstract Full Text Full Text PDF PubMed Scopus (200) Google Scholar). These oscillations lead to a time-averaged polar gradient, in which the lowest levels of the FtsZ inhibitor are found in the cell middle, thus linking cell shape with assembly of its division apparatus (Figure 1). The ability of this system to assess cell geometry predicts changes in its behavior upon alterations to cell size and shape. As such, when cell division is inhibited to generate long bacterial filaments, the MinCDE system appears in vertical stripes along the length of the cell, suggesting the establishment of defined geometric domains (Raskin and de Boer, 1997Raskin D.M. de Boer P.A. Cell. 1997; 91: 685-694Abstract Full Text Full Text PDF PubMed Scopus (200) Google Scholar). As in wild-type cells, the MinCDE stripes are dynamic but move in a coordinated manner consistent with a single signal leading to organized behavior. Moreover, MinCDE can also oscillate in rounded cells and thus does not depend on the rod-like shape of wild-type cells (Corbin et al., 2002Corbin B.D. Yu X.C. Margolin W. EMBO J. 2002; 21: 1998-2008Crossref PubMed Scopus (90) Google Scholar). These results suggested that the MinCDE oscillator provides a read-out of cell geometry, and computational modeling has revealed the potential for these oscillations to result from the self-organization of the three components without the need for additional signals (Kruse et al., 2007Kruse K. Howard M. Margolin W. Mol. Microbiol. 2007; 63: 1279-1284Crossref PubMed Scopus (67) Google Scholar, Lutkenhaus, 2007Lutkenhaus J. Annu. Rev. Biochem. 2007; 76: 539-562Crossref PubMed Scopus (429) Google Scholar). Thus, cell geometry acts as a guide for a self-organized oscillator that then provides a read-out for controlling cell division. The investigative approach used here, which combines experimental understanding of the molecular components with the generation of computational models, provides a good approach for studies of other geometry-sensing mechanisms. This ability to link cell geometry and cell division is not unique to E. coli, and investigations of other bacterial cell types have revealed alternative strategies that achieve the same goal. Geometry sensing in B. subtilis and C. crescentus shares a three-component design principle despite using different proteins. The three key features of these systems are (1) a self-assembling filament anchor at cell ends, (2) an inhibitor of FtsZ, and (3) a molecular adaptor (Figure 1). Mounting evidence suggests that the filament anchors can target the cell ends by preferentially interacting with negatively curved membranes, a notion that is reinforced by their assembly at cell ends when ectopically expressed in other cell types (Bowman et al., 2008Bowman G.R. Comolli L.R. Zhu J. Eckart M. Koenig M. Downing K.H. Moerner W.E. Earnest T. Shapiro L. Cell. 2008; 134: 945-955Abstract Full Text Full Text PDF PubMed Scopus (220) Google Scholar, Ebersbach et al., 2008Ebersbach G. Briegel A. Jensen G.J. Jacobs-Wagner C. Cell. 2008; 134: 956-968Abstract Full Text Full Text PDF PubMed Scopus (209) Google Scholar, Edwards et al., 2000Edwards D.H. Thomaides H.B. Errington J. EMBO J. 2000; 19: 2719-2727Crossref PubMed Scopus (97) Google Scholar, Lenarcic et al., 2009Lenarcic R. Halbedel S. Visser L. Shaw M. Wu L.J. Errington J. Marenduzzo D. Hamoen L.W. EMBO J. 2009; 28: 2272-2282Crossref PubMed Scopus (239) Google Scholar, Ramamurthi and Losick, 2009Ramamurthi K.S. Losick R. Proc. Natl. Acad. Sci. USA. 2009; 106: 13541-13545Crossref PubMed Scopus (190) Google Scholar, Stahlberg et al., 2004Stahlberg H. Kutejova E. Muchova K. Gregorini M. Lustig A. Muller S.A. Olivieri V. Engel A. Wilkinson A.J. Barak I. Mol. Microbiol. 2004; 52: 1281-1290Crossref PubMed Scopus (76) Google Scholar). This suggests a key role for membrane curvature in the organization of cell division control systems, with several such curvature-sensing mechanisms recently proposed (Lenarcic et al., 2009Lenarcic R. Halbedel S. Visser L. Shaw M. Wu L.J. Errington J. Marenduzzo D. Hamoen L.W. EMBO J. 2009; 28: 2272-2282Crossref PubMed Scopus (239) Google Scholar, Ramamurthi et al., 2009Ramamurthi K.S. Lecuyer S. Stone H.A. Losick R. Science. 2009; 323: 1354-1357Crossref PubMed Scopus (158) Google Scholar, Ramamurthi and Losick, 2009Ramamurthi K.S. Losick R. Proc. Natl. Acad. Sci. USA. 2009; 106: 13541-13545Crossref PubMed Scopus (190) Google Scholar). In these organisms, adaptor proteins tether the chromosome to the cell pole while also providing the molecular link between the filament anchors and the inhibitors of FtsZ (Bowman et al., 2008Bowman G.R. Comolli L.R. Zhu J. Eckart M. Koenig M. Downing K.H. Moerner W.E. Earnest T. Shapiro L. Cell. 2008; 134: 945-955Abstract Full Text Full Text PDF PubMed Scopus (220) Google Scholar, Bramkamp et al., 2008Bramkamp M. Emmins R. Weston L. Donovan C. Daniel R.A. Errington J. Mol. Microbiol. 2008; 70: 1556-1569Crossref PubMed Scopus (127) Google Scholar, Ebersbach et al., 2008Ebersbach G. Briegel A. Jensen G.J. Jacobs-Wagner C. Cell. 2008; 134: 956-968Abstract Full Text Full Text PDF PubMed Scopus (209) Google Scholar, Patrick and Kearns, 2008Patrick J.E. Kearns D.B. Mol. Microbiol. 2008; 70: 1166-1179Crossref PubMed Scopus (174) Google Scholar, Thanbichler and Shapiro, 2006Thanbichler M. Shapiro L. Cell. 2006; 126: 147-162Abstract Full Text Full Text PDF PubMed Scopus (349) Google Scholar). B. subtilis uses the same FtsZ inhibitor as E. coli despite different “input” signals related to cell geometry (Marston et al., 1998Marston A.L. Thomaides H.B. Edwards D.H. Sharpe M.E. Errington J. Genes Dev. 1998; 12: 3419-3430Crossref PubMed Scopus (289) Google Scholar). Here, we focus on the role of B. subtilis MinCD at the cell poles for comparison with other geometry-sensing mechanisms, but this protein complex also targets the late division site in a mechanism proposed to prevent Z-ring assembly near existing division septa (Gregory et al., 2008Gregory J.A. Becker E.C. Pogliano K. Genes Dev. 2008; 22: 3475-3488Crossref PubMed Scopus (97) Google Scholar). In C. crescentus, the FtsZ inhibitor is MipZ, which forms a polarized gradient from the cell ends (Thanbichler and Shapiro, 2006Thanbichler M. Shapiro L. Cell. 2006; 126: 147-162Abstract Full Text Full Text PDF PubMed Scopus (349) Google Scholar). Gradients may be a common theme in geometry-sensing mechanisms to generate controls that are adaptable to changes in cell size and shape. These examples illustrate the point that common design principles may have evolved in organisms that use distinct sets of molecular players. These prokaryote examples indicate that cells can monitor their geometry and use this information to generate temporal and spatial control over cell division. But do such mechanisms operate in eukaryotes? Experimental evidence suggests links between cell size and cell division in eukaryotes, but do similar themes and design principles apply? Work from fission and budding yeast indicates that eukaryotic cells possess size-sensing mechanisms linked to controls over cell-cycle transitions, including entry into mitosis. Central to this mitotic control system in fission yeast is the ubiquitous cyclin-dependent kinase Cdk1, which drives entry into mitosis by phosphorylating a wide range of targets, and its inhibitor Wee1, which phosphorylates and inhibits Cdk1 to prevent precocious entry into mitosis (Jorgensen and Tyers, 2004Jorgensen P. Tyers M. Curr. Biol. 2004; 14: R1014-R1027Abstract Full Text Full Text PDF PubMed Scopus (434) Google Scholar, Rupes, 2002Rupes I. Trends Genet. 2002; 18: 479-485Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar). Fission yeast cells are cylindrical and grow in a polarized manner at their tips while maintaining a constant cell width, and this regular cell shape suggests that size-monitoring mechanisms could also involve cell geometry. Mutations in the Cdk1 control system suggest that cells must reach a defined length to trigger mitotic entry, but the mechanisms that link this size with Cdk1 activation are unclear. Recent studies have identified a two-part system that may link cell geometry with Cdk1 regulation (Figure 1) (Martin and Berthelot-Grosjean, 2009Martin S.G. Berthelot-Grosjean M. Nature. 2009; 459: 852-856Crossref PubMed Scopus (233) Google Scholar, Moseley et al., 2009Moseley J.B. Mayeux A. Paoletti A. Nurse P. Nature. 2009; 459: 857-860Crossref PubMed Scopus (284) Google Scholar). First, a set of cortical nodes in the middle of interphase cells contains Wee1 and multiple inhibitors of Wee1, including the Wee1-inhibitory kinase Cdr2. Genetic evidence supports the notion that these nodes promote mitotic entry through negative regulation of Wee1. Second, the protein kinase Pom1 forms a polarized gradient that is enriched at cell ends and inhibits mitotic entry by negatively regulating the cortical nodes. Due to the shape of this gradient, Pom1 overlaps with the cortical nodes in small cells but not in large cells and thus appears to inhibit mitotic entry until cells reach a critical size. Pom1 also participates in additional mechanisms linking cell geometry and cell division in fission yeast by promoting assembly of the cytokinetic ring in the cell middle (Celton-Morizur et al., 2006Celton-Morizur S. Racine V. Sibarita J.B. Paoletti A. J. Cell Sci. 2006; 119: 4710-4718Crossref PubMed Scopus (79) Google Scholar, Padte et al., 2006Padte N.N. Martin S.G. Howard M. Chang F. Curr. Biol. 2006; 16: 2480-2487Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar) and then blocking cytokinesis at cell ends (Huang et al., 2007Huang Y. Chew T.G. Ge W. Balasubramanian M.K. Dev. Cell. 2007; 12: 987-996Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar), a process with intriguing similarities to regulation of the Z-ring in bacteria. This “tip occlusion” of cytokinesis becomes particularly important in small cells, where cell ends are closer together. These examples indicate that multiple steps in the fission yeast cell division process incorporate signals related to cell geometry. This fission yeast system suggests a mechanism that senses cell geometry and may contain design principles related to the bacterial examples. Approaches that elucidated the geometry-sensing mechanisms in bacteria are likely to provide a framework for answering the open questions in this eukaryotic system. For example, what aspect of size is measured by the gradient-node system? As in bacteria, experiments that examine the organization and activity of the system upon changes to cell geometry will indicate whether this mechanism reflects geometry or some other proxy related to cell size. Do the central players self-organize like the MinCDE system in E. coli, or are self-assembling anchors and adaptor proteins involved similar to the B. subtilis and C. crescentus systems? Establishment of the Pom1 gradient requires microtubules (Bahler and Pringle, 1998Bahler J. Pringle J.R. Genes Dev. 1998; 12: 1356-1370Crossref PubMed Scopus (210) Google Scholar), which self-organize into an array in fission yeast cells (Carazo-Salas and Nurse, 2006Carazo-Salas R.E. Nurse P. Nat. Cell Biol. 2006; 8: 1102-1107Crossref PubMed Scopus (60) Google Scholar, Daga et al., 2006Daga R.R. Lee K.G. Bratman S. Salas-Pino S. Chang F. Nat. Cell Biol. 2006; 8: 1108-1113Crossref PubMed Scopus (52) Google Scholar), hinting at self-organization in this system. The self-organizing principle of the MinCDE system became clear through computational models that followed from the identification and characterization of the primary components. Similar models are likely to generate new experimental approaches for understanding the fission yeast system and may suggest how the geometry of cell ends versus the cell middle can organize this gradient-node mechanism. It is possible that the ends of fission yeast cells provide an environment or curvature to organize filament anchors, as shown by the ability of the B. subtilis filament anchor DivIVA to localize at cell ends when ectopically expressed in fission yeast (Edwards et al., 2000Edwards D.H. Thomaides H.B. Errington J. EMBO J. 2000; 19: 2719-2727Crossref PubMed Scopus (97) Google Scholar). This possibility suggests that geometric shapes may generate a universal signal in widely divergent organisms. Several general themes emerge from a comparison of these prokaryotic and eukaryotic geometry-sensing mechanisms. In all cases, polar inhibition is established by molecules at the cell poles that inhibit cell division and can act as sensors of cell geometry. Components that may contribute to these polar cues include self-assembling anchors, cell curvature, and the organization of phospholipids and sterols. The molecular details of these cues and their signaling pathways may vary between cell types and organisms, but the presence of conserved design principles supports the importance of studying the organization and emergent properties of these model systems. Spatial gradients also appear in each system, with the potential for adaptable control of downstream decisions. It will be important to understand how thresholds are set for these gradient-based signals, in particular for controlling mitotic entry in eukaryotic cells. Changes in these gradients and their signaling targets may also contribute to how cells respond to changes in growth conditions or nutrients, which often affect cell division (Jorgensen and Tyers, 2004Jorgensen P. Tyers M. Curr. Biol. 2004; 14: R1014-R1027Abstract Full Text Full Text PDF PubMed Scopus (434) Google Scholar). Ultimately, a systems-level understanding of how cell geometry directs cell division events will emerge from combining genetic, cell biological, biochemical, and computational approaches. Such progress has been successful in bacterial systems such as MinCDE and represents a key future goal for systems in eukaryotic cells such as fission yeast. The described geometry sensors act to trigger events at cell division, when chromosomal DNA must be segregated to opposite cell poles. This segregation relies on cell size and shape, as the mitotic spindle must be oriented to position chromosomes within the defined geometry of the cell. This raises the possibility that geometry sensors might serve the role of delaying cell division until cells have reached an appropriate size and shape to promote proper spindle orientation and elongation. In support of this idea, functional links between cell geometry and the DNA segregation machinery have been described in cell types that display geometry-sensing mechanisms. In fission yeast, cell geometry directs spindle orientation in two ways. During early mitosis, the initial orientation of short spindles follows the alignment of interphase microtubules, which self-organize according to cell geometry along the long axis of these cylindrical cells. At anaphase B, elongating spindles then orient according to cell geometry—the physical constraints of a cylindrical cell align the spindle along the long axis to facilitate segregation of the chromosomes to opposite poles (Daga and Nurse, 2008Daga R.R. Nurse P. J. Cell Sci. 2008; 121: 1973-1980Crossref PubMed Scopus (12) Google Scholar, Vogel et al., 2007Vogel S.K. Raabe I. Dereli A. Maghelli N. Tolic-Norrelykke I. Curr. Biol. 2007; 17: 438-444Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar). As such, changes in cell shape leave cells vulnerable to segregation defects leading to polyploidy. The intriguing connection here is that cells might delay mitotic entry until reaching a specific geometry, which then ensures proper segregation of the genome. A similar connection appears to operate in bacterial cells, where the chromosomes occupy such a large proportion of the cell volume that their segregation inevitably follows the long axis of the cell. This chromosome positioning is exploited by the nucleoid occlusion system to reinforce spatial control of cytokinesis by the Min systems (Bernhardt and de Boer, 2005Bernhardt T.G. de Boer P.A. Mol. Cell. 2005; 18: 555-564Abstract Full Text Full Text PDF PubMed Scopus (385) Google Scholar, Wu and Errington, 2004Wu L.J. Errington J. Cell. 2004; 117: 915-925Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar, Wu et al., 2009Wu L.J. Ishikawa S. Kawai Y. Oshima T. Ogasawara N. Errington J. EMBO J. 2009; 28: 1940-1952Crossref PubMed Scopus (117) Google Scholar). Moreover, additional work has demonstrated the ability of bacterial “spindles” that segregate plasmid DNA and contain the actin-like protein ParM to follow geometric cues both in vitro and in vivo (Campbell and Mullins, 2007Campbell C.S. Mullins R.D. J. Cell Biol. 2007; 179: 1059-1066Crossref PubMed Scopus (76) Google Scholar, Garner et al., 2007Garner E.C. Campbell C.S. Weibel D.B. Mullins R.D. Science. 2007; 315: 1270-1274Crossref PubMed Scopus (166) Google Scholar). Thus, in both fission yeast and bacterial cells, the controls over cell division are linked with mechanisms of spindle orientation and behavior through cell geometry. These examples support the possibility of geometry-sensing mechanisms that control the timing of cell division to ensure proper segregation of the genome. But what about cell types that control division according to different signals? For example, budding yeast cells initiate mitosis through a Wee1 signaling pathway that shares many components with fission yeast, but this budding yeast pathway is not known to use a gradient-based signal and does not appear to monitor geometry. Rather, the budding yeast pathway is proposed to survey the integrity of the bud neck and proper organization of the actin cytoskeleton (Keaton and Lew, 2006Keaton M.A. Lew D.J. Curr. Opin. Microbiol. 2006; 9: 540-546Crossref PubMed Scopus (65) Google Scholar). This difference becomes interesting when one considers the different mechanisms that determine spindle orientation and positioning in these two cell types. Unlike geometry-based positioning of the fission yeast spindle, the budding yeast spindle is pulled from the mother cell into the bud neck along polarized actin cables, which emanate from the daughter cell (Siller and Doe, 2009Siller K.H. Doe C.Q. Nat. Cell Biol. 2009; 11: 365-374Crossref PubMed Scopus (381) Google Scholar). This means that spindle positioning in budding yeast cells requires proper organization of the bud neck and the actin cytoskeleton—the two factors that appear to control cell division timing through Wee1 and Cdk1. This raises the possibility that, in some cell types, checkpoints regulating mitotic entry could be tailored to the mechanisms that control events during cell division. How might these lessons from yeast and bacterial cells relate to animal cells and other multicellular organisms? In such cells, signals controlling progression through the cell cycle are likely to come from both intrinsic (e.g., cell geometry) and extrinsic (e.g., contact inhibition) sources. This contrasts with single-celled organisms such as bacteria and yeast, which act more often through intrinsic, or cell-autonomous, signals with some modulation by environmental cues such as nutritional availability. Cell geometry appears to play at least some role in controlling the cell cycle in animal cells, in part through signaling pathways that respond to cortical tension generated by both cell-cell and cell-matrix interactions (Chen et al., 1997Chen C.S. Mrksich M. Huang S. Whitesides G.M. Ingber D.E. Science. 1997; 276: 1425-1428Crossref PubMed Scopus (4181) Google Scholar). The complexity of distinguishing between intrinsic versus extrinsic cues may have contributed to the long-standing debates over the existence of size control in animal cells. Recent work supports the existence of such size control with implications for signals controlling cell division (Tzur et al., 2009Tzur A. Kafri R. LeBleu V.S. Lahav G. Kirschner M.W. Science. 2009; 325: 167-171Crossref PubMed Scopus (292) Google Scholar), although it remains to be seen how widespread this effect may be for different cell types and organisms. Despite these complications, several lines of evidence suggest that controls over the cell cycle and DNA segregation may be linked in at least some animal cell types. One means of focusing on intrinsic signals in animal cells is to examine the first division in a newly fertilized embryo. Such work in the worm Caenorhabditis elegans has identified polarity proteins that control both mitotic entry and spindle orientation (Rivers et al., 2008Rivers D.M. Moreno S. Abraham M. Ahringer J. J. Cell Biol. 2008; 180: 877-885Crossref PubMed Scopus (63) Google Scholar). In many cell types, including C. elegans embryos, the mitotic spindle is oriented and positioned by interactions between astral microtubules and the cell cortex. In C. elegans, PAR proteins in the cell cortex position the spindle and also control two central regulators of mitotic entry—Cdc25 and Polo kinase. Thus, in animal cells, the control system that decides when to enter mitosis and the control system that orients the mitotic spindle can be linked. As in single-celled organisms, this connection relies on cortical cell polarity proteins, and such polarized pulling forces at the cell cortex can align the mitotic spindle to direct asymmetric divisions. These asymmetric cell divisions can drive cell fate decisions, implicating these connections in cell differentiation and stem cell renewal (Siller and Doe, 2009Siller K.H. Doe C.Q. Nat. Cell Biol. 2009; 11: 365-374Crossref PubMed Scopus (381) Google Scholar). The common link between the mitotic entry control system and spindle orientation appears to be cortical polarity factors, which also facilitate mitotic entry in human cells. Indeed, a growing number of focal adhesion proteins, which contribute to the orientation of cell division by organizing actin stress fibers (Thery et al., 2005Thery M. Racine V. Pepin A. Piel M. Chen Y. Sibarita J.B. Bornens M. Nat. Cell Biol. 2005; 7: 947-953Crossref PubMed Scopus (637) Google Scholar), have been linked to mitotic entry through the Aurora-A kinase (Hirota et al., 2000Hirota T. Morisaki T. Nishiyama Y. Marumoto T. Tada K. Hara T. Masuko N. Inagaki M. Hatakeyama K. Saya H. J. Cell Biol. 2000; 149: 1073-1086Crossref PubMed Scopus (176) Google Scholar, Hirota et al., 2003Hirota T. Kunitoku N. Sasayama T. Marumoto T. Zhang D. Nitta M. Hatakeyama K. Saya H. Cell. 2003; 114: 585-598Abstract Full Text Full Text PDF PubMed Scopus (531) Google Scholar, Pugacheva and Golemis, 2005Pugacheva E.N. Golemis E.A. Nat. Cell Biol. 2005; 7: 937-946Crossref PubMed Scopus (193) Google Scholar, Zhao et al., 2005Zhao Z.S. Lim J.P. Ng Y.W. Lim L. Manser E. Mol. Cell. 2005; 20: 237-249Abstract Full Text Full Text PDF PubMed Scopus (194) Google Scholar). These examples suggest a conserved ability of cortical polarity factors to link cell geometry with mitotic entry and spindle orientation. This may allow the cell to delay entry into mitosis until proper assembly of these polarized cues for spindle orientation and chromosome segregation. We have described a range of mechanisms that monitor cell geometry and link these measurements to mitosis and cell division in different cell types and organisms. This type of cell size control checkpoint differs from others that have been proposed to monitor some surrogate of cell size, such as biosynthetic capacity or protein mass (Jorgensen and Tyers, 2004Jorgensen P. Tyers M. Curr. Biol. 2004; 14: R1014-R1027Abstract Full Text Full Text PDF PubMed Scopus (434) Google Scholar). These types of size control operate at the beginning of the cell cycle, and so this difference may reflect differing requirements for starting a cell cycle versus triggering the end of the cell cycle at cell division. To start a cell cycle, size checkpoints may need to ensure that sufficient resources are available to power through the long haul of a full cell cycle, which includes a range of energy-consuming tasks and cellular growth. At division, different checkpoints may need also to ensure that both the cellular geometry and cortical protein machinery needed for successful mitosis and cytokinesis have been assembled. It is important to note that such geometry sensing is likely to be part of a larger size control system that may include a range of additional input signals. Identification of the input signals that trigger mitotic entry in different cell types or act redundantly within the same cell type may help to illuminate how broadly geometry-sensing mechanisms are used. In multicellular organisms, these intrinsic signals are likely to be additionally coordinated with a range of extrinsic cues related to the extracellular environment." @default.
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• W2009780792 date "2010-07-01" @default.
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• W2009780792 title "Cell Division Intersects with Cell Geometry" @default.
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• W2009780792 doi "https://doi.org/10.1016/j.cell.2010.07.004" @default.
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