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Cell cycle
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For the separation of chromosomes that occurs as part of the cell cycle, see mitosis. For the Academic journal, see Cell Cycle (journal).
See also: Cell division
Life Cycle of the cell
Onion (Allium) cells in different phases of the cell cycle. Growth in an 'organism' is carefully controlled by regulating the cell cycle.
The cell cycle or cell-division cycle is the series of events that take place in a cell leading to its division and duplication of its DNA (DNA replication) to produce two daughter cells. In bacteria, which lack a cell nucleus, the cell cycle is divided into the B, C, and D periods. The B period extends from the end of cell division to the beginning of DNA replication. DNA replication occurs during the C period. The D period refers to the stage between the end of DNA replication and the splitting of the bacterial cell into two daughter cells.[1] In cells with a nucleus, as in eukaryotes, the cell cycle is also divided into three periods: interphase, the mitotic (M) phase, and cytokinesis. During interphase, the cell grows, accumulating nutrients needed for mitosis, preparing it for cell division and duplicating its DNA. During the mitotic phase, the chromosomes separate. During the final stage, cytokinesis, the chromosomes and cytoplasm separate into two new daughter cells. To ensure the proper division of the cell, there are control mechanisms known as cell cycle checkpoints.
The cell-division cycle is a vital process by which a single-celled fertilized egg develops into a mature organism, as well as the process by which hair, skin, blood cells, and some internal organs are renewed. After cell division, each of the daughter cells begin the interphase of a new cycle. Although the various stages of interphase are not usually morphologically distinguishable, each phase of the cell cycle has a distinct set of specialized biochemical processes that prepare the cell for initiation of cell divisions.
Contents
[hide]
1 Phases
1.1 G0 phase (quiescence)
1.2 Interphase (intermitosis)
1.2.1 G1 phase (First growth phase or Post mitotic gap phase)
1.2.2 S phase (DNA replication)
1.2.3 G2 phase (growth)
1.3 Mitotic phase (chromosome separation)
1.4 Cytokinesis phase (separation of all cell components)
2 Regulation of eukaryotic cell cycle
2.1 Role of cyclins and CDKs
2.1.1 General mechanism of cyclin-CDK interaction
2.1.2 Specific action of cyclin-CDK complexes
2.2 Inhibitors
2.3 Transcriptional regulatory network
2.4 DNA replication and DNA replication origin activity
3 Checkpoints
4 Fluorescence imaging of the cell cycle
5 Role in tumor formation
6 See also
7 References
8 Further reading
9 External links
Phases[edit]
The cell cycle consists of four distinct phases: G1 phase, S phase (synthesis), G2 phase (collectively known as interphase) and M phase (mitosis). M phase is itself composed of two tightly coupled processes: karyokinesis, in which the cell's chromosomes are divided, and cytokinesis, in which the cell's cytoplasm divides forming two daughter cells. Activation of each phase is dependent on the proper progression and completion of the previous one. Cells that have temporarily or reversibly stopped dividing are said to have entered a state of quiescence called G0 phase.
Schematic of the cell cycle. outer ring: I = Interphase, M = Mitosis; inner ring: M = Mitosis, G1 = Gap 1, G2 = Gap 2, S = Synthesis; not in ring: G0 = Gap 0/Resting.[2]
State
Phase
Abbreviation
Description
Resting Gap 0 G0 A phase where the cell has left the cycle and has stopped dividing.
Interphase Gap 1 G1 Cells increase in size in Gap 1. The G1 checkpoint control mechanism ensures that everything is ready for DNA synthesis.
Synthesis S DNA replication occurs during this phase.
Gap 2 G2 During the gap between DNA synthesis and mitosis, the cell will continue to grow. The G2 checkpoint control mechanism ensures that everything is ready to enter the M (mitosis) phase and divide.
Cell division Mitosis M Cell growth stops at this stage and cellular energy is focused on the orderly division into two daughter cells. A checkpoint in the middle of mitosis (Metaphase Checkpoint) ensures that the cell is ready to complete cell division.
After cell division, each of the daughter cells begin the interphase of a new cycle. Although the various stages of interphase are not usually morphologically distinguishable, each phase of the cell cycle has a distinct set of specialized biochemical processes that prepare the cell for initiation of cell division.
G0 phase (quiescence)[edit]
Plant cell cycle
Animal cell cycle
G0 is a resting phase where the cell has left the cycle and has stopped dividing. The cell cycle starts with this phase. The word "post-mitotic" is sometimes used to refer to both quiescent and senescent cells. Non-proliferative (non-dividing) cells in multicellular eukaryotes generally enter the quiescent G0 state from G1 and may remain quiescent for long periods of time, possibly indefinitely (as is often the case for neurons). This is very common for cells that are fully differentiated. Cellular senescence occurs in response to DNA damage and external stress and usually constitutes an arrest in G1. Some cells enter the G0 phase semi-permanently and are considered post-mitotic, e.g., some liver, kidney, and stomach cells. Many cells do not enter G0 and continue to divide throughout an organism's life, e.g., epithelial cells.
Cellular senescence is also a state that occurs in response to DNA damage or degradation that would make a cell's progeny nonviable; it is often a biochemical alternative to the self-destruction of such a damaged cell by apoptosis.
Interphase (intermitosis)[edit]
Before a cell can enter cell division, it needs to take in nutrients. All of the preparations are done during interphase. Interphase is a series of changes that takes place in a newly formed cell and its nucleus, before it becomes capable of division again. It is also called preparatory phase or intermitosis. Previously it was called resting stage because there is no apparent activity related to cell division.Typically interphase lasts for at least 91% of the total time required for the cell cycle.
Interphase proceeds in three stages, G1, S, and G2, followed by the cycle of mitosis and cytokinesis. The cell's nuclear DNA contents are duplicated during S phase but may continue till G2 in case of heterochromatin.
G1 phase (First growth phase or Post mitotic gap phase)[edit]
The first phase within interphase, from the end of the previous M phase until the beginning of DNA synthesis, is called G1 (G indicating gap). It is also called the growth phase. During this phase, the biosynthetic activities of the cell, which are considerably slowed down during M phase, resume at a high rate. The duration of G1 is highly variable, even among different cells of the same species.[3] In this phase, the cell increases its supply of proteins, increases the number of organelles (such as mitochondria, ribosomes), and grows in size. In G1 phase, a cell has three options. (1) To continue cell cycle and enter S phase (2) Stop cell cycle and enter G0 phase for undergoing differentiation. (3) Get arrested in G1 phase hence it may enter G0 phase or re-enter cell cycle. The deciding factor is availability of nitrogens and storage of energy rich compounds at the deciding point called check point. This check point is called G1 cyclin or CG1. It causes transition of G1 to S phase. Once the check point of G1 phase is crossed, cell cycle will go uninterrupted till it is completed.
S phase (DNA replication)[edit]
The ensuing S phase starts when DNA synthesis commences; when it is complete, all of the chromosomes have been replicated, i.e., each chromosome has two (sister) chromatids. Thus, during this phase, the amount of DNA in the cell has effectively doubled, though the ploidy of the cell remains the same. Rates of RNA transcription and protein synthesis are very low during this phase. An exception to this is histone production, most of which occurs during the S phase.[4][5][6]
G2 phase (growth)[edit]
G2 phase occurs after DNA replication and is a period of protein synthesis and rapid cell growth to prepare the cell for mitosis. During this phase microtubules begin to reorganize to form a spindle.
Mitotic phase (chromosome separation)[edit]
Main article: Mitosis
The relatively brief M phase consists of nuclear division (karyokinesis). It is a relatively short period of the cell cycle. M phase is complex and highly regulated. The sequence of events is divided into phases, corresponding to the completion of one set of activities and the start of the next. These phases are sequentially known as:
prophase,
metaphase,
anaphase,
telophase
Mitosis is the process by which a eukaryotic cell separates the chromosomes in its cell nucleus into two identical sets in two nuclei.[7] During the process of mitosis the pairs of chromosomes condense and attach to fibers that pull the sister chromatids to opposite sides of the cell.[8]
Mitosis occurs exclusively in eukaryotic cells, but occurs in different ways in different species. For example, animals undergo an "open" mitosis, where the nuclear envelope breaks down before the chromosomes separate, while fungi such as Aspergillus nidulans and Saccharomyces cerevisiae (yeast) undergo a "closed" mitosis, where chromosomes divide within an intact cell nucleus.[9] Prokaryotic cells, which lack a nucleus, divide by a process called binary fission.
Cytokinesis phase (separation of all cell components)[edit]
Main article: Cytokinesis
Mitosis is immediately followed by cytokinesis, which divides the nuclei, cytoplasm, organelles and cell membrane into two cells containing roughly equal shares of these cellular components. Mitosis and cytokinesis together define the division of the mother cell into two daughter cells, genetically identical to each other and to their parent cell. This accounts for approximately 10% of the cell cycle.
Because cytokinesis usually occurs in conjunction with mitosis, "mitosis" is often used interchangeably with "M phase". However, there are many cells where mitosis and cytokinesis occur separately, forming single cells with multiple nuclei in a process called endoreplication. This occurs most notably among the fungi and slime moulds, but is found in various groups. Even in animals, cytokinesis and mitosis may occur independently, for instance during certain stages of fruit fly embryonic development.[10] Errors in mitosis can either kill a cell through apoptosis or cause mutations that may lead to cancer.
The process of mitosis is complex and highly regulated. The sequence of events is divided into phases, corresponding to the completion of one set of activities and the start of the next. These stages are prophase, prometaphase, metaphase, anaphase and telophase. During the process of mitosis the pairs of chromosomes condense and attach to fibers that pull the sister chromatids to opposite sides of the cell. The cell then divides in cytokinesis, to produce two identical daughter cells.[8]
Regulation of eukaryotic cell cycle[edit]
Regulation of the cell cycle involves processes crucial to the survival of a cell, including the detection and repair of genetic damage as well as the prevention of uncontrolled cell division. The molecular events that control the cell cycle are ordered and directional; that is, each process occurs in a sequential fashion and it is impossible to "reverse" the cycle.
Role of cyclins and CDKs[edit]

Nobel Laureate
Paul Nurse
Nobel Laureate
Tim Hunt
Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the cell cycle.[11] Leland H. Hartwell, R. Timothy Hunt, and Paul M. Nurse won the 2001 Nobel Prize in Physiology or Medicine for their discovery of these central molecules.[12] Many of the genes encoding cyclins and CDKs are conserved among all eukaryotes, but in general more complex organisms have more elaborate cell cycle control systems that incorporate more individual components. Many of the relevant genes were first identified by studying yeast, especially Saccharomyces cerevisiae;[13] genetic nomenclature in yeast dubs many of these genes cdc (for "cell division cycle") followed by an identifying number, e.g. cdc25 or cdc20.
Cyclins form the regulatory subunits and CDKs the catalytic subunits of an activated heterodimer; cyclins have no catalytic activity and CDKs are inactive in the absence of a partner cyclin. When activated by a bound cyclin, CDKs perform a common biochemical reaction called phosphorylation that activates or inactivates target proteins to orchestrate coordinated entry into the next phase of the cell cycle. Different cyclin-CDK combinations determine the downstream proteins targeted. CDKs are constitutively expressed in cells whereas cyclins are synthesised at specific stages of the cell cycle, in response to various molecular signals.[14]
General mechanism of cyclin-CDK interaction[edit]
Upon receiving a pro-mitotic extracellular signal, G1 cyclin-CDK complexes become active to prepare the cell for S phase, promoting the expression of transcription factors that in turn promote the expression of S cyclins and of enzymes required for DNA replication. The G1 cyclin-CDK complexes also promote the degradation of molecules that function as S phase inhibitors by targeting them for ubiquitination. Once a protein has been ubiquitinated, it is targeted for proteolytic degradation by the proteasome. However, results from a recent study of E2F transcriptional dynamics at the single-cell level argue that the role of G1 cyclin-CDK activities, in particular cyclin D-CDK4/6, is to tune the timing rather than the commitment of cell cycle entry.[15]
Active S cyclin-CDK complexes phosphorylate proteins that make up the pre-replication complexes assembled during G1 phase on DNA replication origins. The phosphorylation serves two purposes: to activate each already-assembled pre-replication complex, and to prevent new complexes from forming. This ensures that every portion of the cell's genome will be replicated once and only once. The reason for prevention of gaps in replication is fairly clear, because daughter cells that are missing all or part of crucial genes will die. However, for reasons related to gene copy number effects, possession of extra copies of certain genes is also deleterious to the daughter cells.
Mitotic cyclin-CDK complexes, which are synthesized but inactivated during S and G2 phases, promote the initiation of mitosis by stimulating downstream proteins involved in chromosome condensation and mitotic spindle assembly. A critical complex activated during this process is a ubiquitin ligase known as the anaphase-promoting complex (APC), which promotes degradation of structural proteins associated with the chromosomal kinetochore. APC also targets the mitotic cyclins for degradation, ensuring that telophase and cytokinesis can proceed.[16]
Specific action of cyclin-CDK complexes[edit]
Cyclin D is the first cyclin produced in the cell cycle, in response to extracellular signals (e.g. growth factors). Cyclin D binds to existing CDK4, forming the active cyclin D-CDK4 complex. Cyclin D-CDK4 complex in turn phosphorylates the retinoblastoma susceptibility protein (Rb). The hyperphosphorylated Rb dissociates from the E2F/DP1/Rb complex (which was bound to the E2F responsive genes, effectively "blocking" them from transcription), activating E2F. Activation of E2F results in transcription of various genes like cyclin E, cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which pushes the cell from G1 to S phase (G1/S, which initiates the G2/M transition).[17] Cyclin B-cdk1 complex activation causes breakdown of nuclear envelope and initiation of prophase, and subsequently, its deactivation causes the cell to exit mitosis.[14] A quantitative study of E2F transcriptional dynamics at the single-cell level by using engineered fluorescent reporter cells provided a quantitative framework for understanding the control logic of cell cycle entry, challenging the canonical textbook model. Genes that regulate the amplitude of E2F accumulation, such as Myc, determine the commitment in cell cycle and S phase entry. G1 cyclin-CDK activities are not the driver of cell cycle entry. Instead, they primarily tune the timing of E2F increase, thereby modulating the pace of cell cycle progression.[15]
Inhibitors[edit]
Overview of signal transduction pathways involved in apoptosis, also known as "programmed cell death".
Two families of genes, the cip/kip (CDK interacting protein/Kinase inhibitory protein) family and the INK4a/ARF (Inhibitor of Kinase 4/Alternative Reading Frame) family, prevent the progression of the cell cycle. Because these genes are instrumental in prevention of tumor formation, they are known as tumor suppressors.
The cip/kip family includes the genes p21, p27 and p57. They halt cell cycle in G1 phase, by binding to, and inactivating, cyclin-CDK complexes. p21 is activated by p53 (which, in turn, is triggered by DNA damage e.g. due to radiation). p27 is activated by Transforming Growth Factor of β (TGF β), a growth inhibitor.
The INK4a/ARF family includes p16INK4a, which binds to CDK4 and arrests the cell cycle in G1 phase, and p14ARF which prevents p53 degradation.
Synthetic inhibitors of Cdc25 could also be useful for the arrest of cell cycle and therefore be useful as antineoplastic and anticancer agents.[18]
Transcriptional regulatory network[edit]
Current evidence suggests that a semi-autonomous transcriptional network acts in concert with the CDK-cyclin machinery to regulate the cell cycle. Several gene expression studies in Saccharomyces cerevisiae have identified 800–1200 genes that change expression over the course of the cell cycle.[13][19][20] They are transcribed at high levels at specific points in the cell cycle, and remain at lower levels throughout the rest of the cycle. While the set of identified genes differs between studies due to the computational methods and criteria used to identify them, each study indicates that a large portion of yeast genes are temporally regulated.[21]
Many periodically expressed genes are driven by transcription factors that are also periodically expressed. One screen of single-gene knockouts identified 48 transcription factors (about 20% of all non-essential transcription factors) that show cell cycle progression defects.[22] Genome-wide studies using high throughput technologies have identified the transcription factors that bind to the promoters of yeast genes, and correlating these findings with temporal expression patterns have allowed the identification of transcription factors that drive phase-specific gene expression.[19][23] The expression profiles of these transcription factors are driven by the transcription factors that peak in the prior phase, and computational models have shown that a CDK-autonomous network of these transcription factors is sufficient to produce steady-state oscillations in gene expression).[20][24]
Experimental evidence also suggests that gene expression can oscillate with the period seen in dividing wild-type cells independently of the CDK machinery. Orlando et al. used microarrays to measure the expression of a set of 1,271 genes that they identified as periodic in both wild type cells and cells lacking all S-phase and mitotic cyclins (clb1,2,3,4,5,6). Of the 1,271 genes assayed, 882 continued to be expressed in the cyclin-deficient cells at the same time as in the wild type cells, despite the fact that the cyclin-deficient cells arrest at the border between G1 and S phase. However, 833 of the genes assayed changed behavior between the wild type and mutant cells, indicating that these genes are likely directly or indirectly regulated by the CDK-cyclin machinery. Some genes that continued to be expressed on time in the mutant cells were also expressed at different levels in the mutant and wild type cells. These findings suggest that while the transcriptional network may oscillate independently of the CDK-cyclin oscillator, they are coupled in a manner that requires both to ensure the proper timing of cell cycle events.[20] Other work indicates that phosphorylation, a post-translational modification, of cell cycle transcription factors by Cdk1 may alter the localization or activity of the transcription factors in order to tightly control timing of target genes.[22][25][26]
While oscillatory transcription plays a key role in the progression of the yeast cell cycle, the CDK-cyclin machinery operates independently in the early embryonic cell cycle. Before the midblastula transition, zygotic transcription does not occur and all needed proteins, such as the B-type cyclins, are translated from maternally loaded mRNA.[27]
DNA replication and DNA replication origin activity[edit]
Analyses of synchronized cultures of Saccharomyces cerevisiae under conditions that prevent DNA replication initiation without delaying cell cycle progression showed that origin licensing decreases the expression of genes with origins near their 3' ends, revealing that downstream origins can regulate the expression of upstream genes.[28] This confirms previous predictions from mathematical modeling of a global causal coordination between DNA replication origin activity and mRNA expression,[29][30][31] and shows that mathematical modeling of DNA microarray data can be used to correctly predict previously unknown biological modes of regulation.
Checkpoints[edit]
Main article: Cell cycle checkpoint
Cell cycle checkpoints are used by the cell to monitor and regulate the progress of the cell cycle.[32] Checkpoints prevent cell cycle progression at specific points, allowing verification of necessary phase processes and repair of DNA damage. The cell cannot proceed to the next phase until checkpoint requirements have been met. Checkpoints typically consist of a network of regulatory proteins that monitor and dictate the progression of the cell through the different stages of the cell cycle.
There are several checkpoints to ensure that damaged or incomplete DNA is not passed on to daughter cells. Three main checkpoints exist: the G1/S checkpoint, the G2/M checkpoint and the metaphase (mitotic) checkpoint.
G1/S transition is a rate-limiting step in the cell cycle and is also known as restriction point.[14] This is where the cell checks whether it has enough raw materials to fully replicate its DNA (nucleotide bases, DNA synthase, chromatin, etc.). An unhealthy or malnourished cell will get stuck at this checkpoint.
The G2/M checkpoint is where the cell ensures that it has enough cytoplasm and phospholipids for two daughter cells. But sometimes more importantly, it checks to see if it is the right time to replicate. There are some situations where many cells need to all replicate simultaneously (for example, a growing embryo should have a symmetric cell distribution until it reaches the mid-blastula transition). This is done by controlling the G2/M checkpoint.
The metaphase checkpoint is a fairly minor checkpoint, in that once a cell is in metaphase, it has committed to undergoing mitosis. However that's not to say it isn't important. In this checkpoint, the cell checks to ensure that the spindle has formed and that all of the chromosomes are aligned at the spindle equator before anaphase begins.[33]
While these are the three "main" checkpoints, not all cells have to pass through each of these checkpoints in this order to replicate. Many types of cancer are caused by mutations that allow the cells to speed through the various checkpoints or even skip them altogether. Going from S to M to S phase almost consecutively. Because these cells have lost their checkpoints, any DNA mutations that may have occurred are disregarded and passed on to the daughter cells. This is one reason why cancer cells have a tendency to exponentially accrue mutations. Aside from cancer cells, many fully differentiated cell types no longer replicate so they leave the cell cycle and stay in G0 until their death. Thus removing the need for cellular checkpoints. An alternative model of the cell cycle response to DNA damage has also been proposed, known as the postreplication checkpoint.
Checkpoint regulation plays an important role in an organism's development. In sexual reproduction, when egg fertilization occurs, when the sperm binds to the egg, it releases signalling factors that notify the egg that it has been fertilized. Among other things, this induces the now fertilized oocyte to return from its previously dormant, G0, state back into the cell cycle and on to mitotic replication and division.
p53 plays an important role in triggering the control mechanisms at both G1/S and G2/M checkpoints. In addition to p53, checkpoint regulators are being heavily researched for their roles in cancer growth and proliferation.
Fluorescence imaging of the cell cycle[edit]
Fluorescent proteins visualize the cell cycle progression. IFP2.0-hGem(1/110) fluorescence is shown in green and highlights the S/G2/M phases. smURFP-hCdtI(30/120) fluorescence is shown in red and highlights the G0/G1 phases.
Pioneering work by Atsushi Miyawaki and coworkers developed the fluorescent ubiquitination-based cell cycle indicator (FUCCI), which enables fluorescence imaging of the cell cycle. Originally, a green fluorescent protein, mAG, was fused to hGem(1/110) and an orange fluorescent protein (mKO2) was fused to hCdt1(30/120). Note, these fusions are fragments that contain a nuclear localization signal and ubiquitination sites for degradation, but are not functional proteins. The green fluorescent protein is made during the S, G2, or M phase and degraded during the G0 or G1 phase, while the orange fluorescent protein is made during the G0 or G1 phase and destroyed during the S, G2, or M phase.[34] A far-red and near-infrared FUCCI was developed using a cyanobacteria-derived fluorescent protein (smURFP) and a bacteriophytochrome-derived fluorescent protein (movie found at this link).[35]
Role in tumor formation[edit]
A disregulation of the cell cycle components may lead to tumor formation.[36] As mentioned above, when some genes like the cell cycle inhibitors, RB, p53 etc. mutate, they may cause the cell to multiply uncontrollably, forming a tumor. Although the duration of cell cycle in tumor cells is equal to or longer than that of normal cell cycle, the proportion of cells that are in active cell division (versus quiescent cells in G0 phase) in tumors is much higher than that in normal tissue[citation needed]. Thus there is a net increase in cell number as the number of cells that die by apoptosis or senescence remains the same.
The cells which are actively undergoing cell cycle are targeted in cancer therapy as the DNA is relatively exposed during cell division and hence susceptible to damage by drugs or radiation. This fact is made use of in cancer treatment; by a process known as debulking, a significant mass of the tumor is removed which pushes a significant number of the remaining tumor cells from G0 to G1 phase (due to increased availability of nutrients, oxygen, growth factors etc.). Radiation or chemotherapy following the debulking procedure kills these cells which have newly entered the cell cycle.[14]
The fastest cycling mammalian cells in culture, crypt cells in the intestinal epithelium, have a cycle time as short as 9 to 10 hours. Stem cells in resting mouse skin may have a cycle time of more than 200 hours. Most of this difference is due to the varying length of G1, the most variable phase of the cycle. M and S do not vary much.
In general, cells are most radiosensitive in late M and G2 phases and most resistant in late S phase.
For cells with a longer cell cycle time and a significantly long G1 phase, there is a second peak of resistance late in G1.
The pattern of resistance and sensitivity correlates with the level of sulfhydryl compounds in the cell. Sulfhydryls are natural substances that protect cells from radiation damage and tend to be at their highest levels in S and at their lowest near mitosis.
See also[edit]
Cellular model
Synchronous culture – synchronization of cell cultures
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Jump up ^ Ubersax JA, Woodbury EL, Quang PN, Paraz M, Blethrow JD, Shah K, Shokat KM, Morgan DO (October 2003). "Targets of the cyclin-dependent kinase Cdk1". Nature. 425 (6960): 859–64. Bibcode:2003Natur.425..859U. doi:10.1038/nature02062. PMID 14574415.
Jump up ^ Morgan DO (2007). "2–3". The Cell Cycle: Principles of Control. London: New Science Press. p. 18. ISBN 0-9539181-2-2.
Jump up ^ Omberg L, Meyerson JR, Kobayashi K, Drury LS, Diffley JF, Alter O (October 2009). "Global effects of DNA replication and DNA replication origin activity on eukaryotic gene expression". Molecular Systems Biology. 5: 312. doi:10.1038/msb.2009.70. PMC 2779084  . PMID 19888207.
Jump up ^ Alter O, Golub GH, Brown PO, Botstein D (2004). Deutscher MP, Black S, Boehmer PE, D'Urso G, Fletcher TM, Huijing F, Marshall A, Pulverer B, Renault B, Rosenblatt JD, Slingerland JM, Whelan WJ, eds. "Novel Genome-Scale Correlation between DNA Replication and RNA Transcription During the Cell Cycle in Yeast is Predicted by Data-Driven Models" (PDF). Miami Nature Biotechnology Winter Symposium: Cell Cycle, Chromosomes and Cancer. Miami Beach, FL: University of Miami School of Medicine, vol. 15 (January 31 – February 4, 2004).
Jump up ^ Alter O, Golub GH (November 2004). "Integrative analysis of genome-scale data by using pseudoinverse projection predicts novel correlation between DNA replication and RNA transcription". Proceedings of the National Academy of Sciences of the United States of America. 101 (47): 16577–82. doi:10.1073/pnas.0406767101. PMC 534520  . PMID 15545604.
Jump up ^ Omberg L, Golub GH, Alter O (November 2007). "A tensor higher-order singular value decomposition for integrative analysis of DNA microarray data from different studies". Proceedings of the National Academy of Sciences of the United States of America. 104 (47): 18371–6. Bibcode:2007PNAS..10418371O. doi:10.1073/pnas.0709146104. PMC 2147680  . PMID 18003902.
Jump up ^ Elledge SJ (December 1996). "Cell cycle checkpoints: preventing an identity crisis". Science. 274 (5293): 1664–72. Bibcode:1996Sci...274.1664E. doi:10.1126/science.274.5293.1664. PMID 8939848.
Jump up ^ LeMaire-Adkins R, Radke K, Hunt PA (December 1997). "Lack of checkpoint control at the metaphase/anaphase transition: a mechanism of meiotic nondisjunction in mammalian females". The Journal of Cell Biology. 139 (7): 1611–9. doi:10.1083/jcb.139.7.1611. PMC 2132649  . PMID 9412457.
Jump up ^ Sakaue-Sawano A, Kurokawa H, Morimura T, Hanyu A, Hama H, Osawa H, Kashiwagi S, Fukami K, Miyata T, Miyoshi H, Imamura T, Ogawa M, Masai H, Miyawaki A (February 2008). "Visualizing spatiotemporal dynamics of multicellular cell-cycle progression". Cell. 132 (3): 487–98. doi:10.1016/j.cell.2007.12.033. PMID 18267078.
Jump up ^ Rodriguez EA, Tran GN, Gross LA, Crisp JL, Shu X, Lin JY, Tsien RY (September 2016). "A far-red fluorescent protein evolved from a cyanobacterial phycobiliprotein". Nature Methods. 13 (9): 763–9. doi:10.1038/nmeth.3935. PMC 5007177  . PMID 27479328.
Jump up ^ Champeris Tsaniras S, Kanellakis N, Symeonidou IE, Nikolopoulou P, Lygerou Z, Taraviras S (June 2014). "Licensing of DNA replication, cancer, pluripotency and differentiation: an interlinked world?". Seminars in Cell & Developmental Biology. 30: 174–80. doi:10.1016/j.semcdb.2014.03.013. PMID 24641889.
Further reading[edit]
Morgan DO (2007). The Cell Cycle: Principles of Control. London: Published by New Science Press in association with Oxford University Press. ISBN 0-87893-508-8.
Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2008). "Chapter 17". Molecular Biology of the Cell (5th ed.). New York: Garland Science. ISBN 978-0-8153-4111-6.
Krieger M, Scott MP, Matsudaira PT, Lodish HF, Darnell JE, Zipursky L, Kaiser C, Berk A (2004). Molecular cell biology. New York: W.H. Freeman and CO. ISBN 0-7167-4366-3.
Watson JD, Baker TA, Bell SP, Gann A, Levine M, Losick R (2004). "Chapter 7". Molecular biology of the gene (5th ed.). San Francisco: Pearson/Benjamin Cummings. ISBN 0-8053-4642-2.
External links[edit]
Wikimedia Commons has media related to Cell cycle.
This article incorporates public domain material from the NCBI document "Science Primer".
David Morgan's seminar: Controlling the Cell Cycle
The cell cycle & Cell death
Transcriptional program of the cell cycle: high-resolution timing
Cell cycle and metabolic cycle regulated transcription in yeast
Cell Cycle Animation 1Lec.com
Cell Cycle
Fucci:Using GFP to visualize the cell-cycle
Science Creative Quarterly's overview of the cell cycle
KEGG – Human Cell Cycle
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text:
Arnold Palmer Invitational
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Arnold Palmer Invitational
Tournament information
Location
Bay Hill, Florida, U.S.
Established
1966, 52 years ago
Course(s)
Bay Hill Club and Lodge
(1979–present)
Par
72
Length
7,419 yards (6,784 m)
Tour(s)
PGA Tour
Format
Stroke play
Prize fund
$8.9 million
Month played
March
Tournament record score
Aggregate
264 Payne Stewart (1987)
To par
−23 Buddy Allin (1973)
Current champion
Rory McIlroy
Bay Hill
Location in the United States
Bay
Hill
Location in Florida
The Arnold Palmer Invitational is a professional golf tournament in Florida on the PGA Tour. It is played each March at the Bay Hill Club and Lodge, a private golf resort owned since 1974 by Arnold Palmer in Bay Hill, a suburb southwest of Orlando.
The event was founded in 1979 as a successor to the Florida Citrus Open Invitational, which debuted in 1966 and was played at Rio Pinar Country Club, east of Orlando, through 1978. Arnold Palmer himself would win the Florida Citrus Open in 1971. Gary Koch would win the Florida Citrus Open in 1977, and then win the Bay Hill Classic in 1984, giving him the very unique distinction of being this event's only winner under its original (1966-1978) and current (1979-present) incarnations.
Since 1979, the tournament title has had a number of different names, most of them including "Bay Hill," but has played under the Palmer name since 2007. On March 21, 2012, the Arnold Palmer Invitational and MasterCard Worldwide announced an extension to MasterCard's "Presented by" sponsorship until the 2016 tournament.[1][2]
Tiger Woods won four years in a row at Bay Hill, from 2000 to 2003, one of only four occasions that an event was won four consecutive times on the PGA Tour. In 2004, he was one shot off the lead after opening with a 67, but followed up with consecutive 74s on Friday and Saturday, and tied for 46th place. Woods also won the 2008 and 2009 tournaments, both times with birdie putts on the final hole. He then won the tournament in 2012 by five shots, his first official PGA Tour win in 924 days and his seventh win at the event. Woods repeated in 2013 for his eighth victory at the tournament. He withdrew two days before the 2014 event, citing a bad back, and underwent surgery shortly after.
Contents
[hide]
1 Invitational status
2 Field
3 Course layout
4 Winners
5 Multiple winners
6 Tournament highlights
7 References
8 External links
Invitational status[edit]
The Arnold Palmer Invitational is one of only five tournaments given "invitational" status by the PGA Tour, and consequently it has a reduced field of only 120 players (as opposed to most full-field open tournaments with a field of 156 players). The other four tournaments with invitational status are the RBC Heritage, the Fort Worth Invitational, the Memorial Tournament, and the Quicken Loans National. Invitational tournaments have smaller fields (between 120 and 132 players), and have more freedom than full-field open tournaments in determining which players are eligible to participate in their event, as invitational tournaments are not required to fill their fields using the PGA Tour Priority Ranking System. Furthermore, unlike full-field open tournaments, invitational tournaments do not offer open qualifying (aka Monday qualifying).
In June 2014, the PGA Tour approved a resolution to grant the winner a three-year exemption, one more than other regular Tour events and on par with winners of the World Golf Championships, The Tour Championship, and the Memorial Tournament.[3]
Field[edit]
The field consists of 120 players invited using the following criteria:[4]
Arnold Palmer Invitational winners prior to 2000 and in the last five years
The Players Championship and major championship winners in the last five years
The Tour Championship, World Golf Championships, and Memorial Tournament winners in the past three years
Tournament winners in the past year
Playing member of last named U.S. Ryder Cup team; current PGA Tour members who were playing members on last named European Ryder Cup team, U.S. Presidents Cup team, and International Presidents Cup team
Prior year U.S. Amateur winner (if still an amateur)
Top 50 Official World Golf Ranking (as of Friday prior)
PGA Tour life members
18 sponsors exemptions– 2 from Web.com Tour finals, 8 members not otherwise exempt, and 8 unrestricted
Up to two foreign players designated by the commissioner
Top 70 from prior year's FedEx Cup points list
Members in top 125 non-member category whose prior year non-WGC points equal or exceed the 70th position on the prior year FedEx Cup points list
Top 70 from current year's FedEx Cup points list (as of Friday prior)
PGA Section champion/player of the year
Remaining positions filled from current year's FedEx Cup points list
Arnold Palmer had a lifetime invitation.
Course layout[edit]
Main article: Bay Hill Club and Lodge
Hole
1
2
3
4
5
6
7
8
9
Out
10
11
12
13
14
15
16
17
18
In
Total
Yards 461 231 434 561 390 555 199 460 474 3,765 400 438 574 370 215 467 511 221 458 3,654 7,419
Par 4 3 4 5 4 5 3 4 4 36 4 4 5 4 3 4 5 3 4 36 72
Source:[5]
Winners[edit]
Year
Player
Country
Score
To par
Margin
of victory
Runner(s)-up
Winner's
share ($)
Purse ($)
Arnold Palmer Invitational presented by MasterCard
2018 Rory McIlroy Northern Ireland 270 −18 3 strokes Bryson DeChambeau 1,602,000 8,900,000
2017 Marc Leishman Australia 277 −11 1 stroke Charley Hoffman
Kevin Kisner 1,566,000 8,700,000
2016 Jason Day Australia 271 −17 1 stroke Kevin Chappell 1,134,000 6,300,000
2015 Matt Every (2) United States 269 −19 1 stroke Henrik Stenson 1,134,000 6,300,000
2014 Matt Every United States 275 −13 1 stroke Keegan Bradley 1,116,000 6,200,000
2013 Tiger Woods (8) United States 275 −13 2 strokes Justin Rose 1,116,000 6,200,000
2012 Tiger Woods (7) United States 275 −13 5 strokes Graeme McDowell 1,080,000 6,000,000
2011 Martin Laird Scotland 280 −8 1 stroke Steve Marino 1,080,000 6,000,000
2010 Ernie Els (2) South Africa 277 −11 2 strokes Edoardo Molinari
Kevin Na 1,080,000 6,000,000
2009 Tiger Woods (6) United States 275 −5 1 stroke Sean O'Hair 1,080,000 6,000,000
2008 Tiger Woods (5) United States 270 −10 1 stroke Bart Bryant 1,044,000 5,800,000
2007 Vijay Singh Fiji 272 −8 2 strokes Rocco Mediate 990,000 5,500,000
Bay Hill Invitational presented by MasterCard
2006 Rod Pampling Australia 274 −14 1 stroke Greg Owen 990,000 5,500,000
2005 Kenny Perry United States 276 −12 2 strokes Graeme McDowell
Vijay Singh 900,000 5,000,000
2004 Chad Campbell United States 270 −18 6 strokes Stuart Appleby 900,000 5,000,000
Bay Hill Invitational presented by Cooper Tires
2003 Tiger Woods (4) United States 269 −19 11 strokes Stewart Cink
Brad Faxon
Kenny Perry
Kirk Triplett 810,000 4,500,000
2002 Tiger Woods (3) United States 275 −13 4 strokes Michael Campbell 720,000 4,000,000
2001 Tiger Woods (2) United States 273 −15 1 stroke Phil Mickelson 630,000 3,500,000
2000 Tiger Woods United States 270 −18 4 strokes Davis Love III 540,000 3,000,000
1999 Tim Herron United States 274 −14 Playoff Tom Lehman 450,000 2,500,000
Bay Hill Invitational presented by Office Depot
1998 Ernie Els South Africa 274 −14 4 strokes Bob Estes
Jeff Maggert 360,000 2,000,000
1997 Phil Mickelson United States 272 −16 3 strokes Stuart Appleby 270,000 1,500,000
1996 Paul Goydos United States 275 −13 1 stroke Jeff Maggert 216,000 1,200,000
Nestle Invitational
1995 Loren Roberts (2) United States 272 −16 2 strokes Brad Faxon 216,000 1,200,000
1994 Loren Roberts United States 275 −13 1 stroke Nick Price
Vijay Singh
Fuzzy Zoeller 216,000 1,200,000
1993 Ben Crenshaw United States 280 −8 2 strokes Davis Love III
Rocco Mediate
Vijay Singh 180,000 1,000,000
1992 Fred Couples United States 269 −19 9 strokes Gene Sauers 180,000 1,000,000
1991 Andrew Magee United States 203* −13 2 strokes Tom Sieckmann 180,000 1,000,000
1990 Robert Gamez United States 274 −14 1 stroke Greg Norman 162,000 900,000
1989 Tom Kite (2) United States 278 −6 Playoff Davis Love III 144,000 800,000
Hertz Bay Hill Classic
1988 Paul Azinger United States 271 −13 5 strokes Tom Kite 135,000 750,000
1987 Payne Stewart United States 264 −20 3 strokes David Frost 108,000 600,000
1986 Dan Forsman United States 202* −11 1 stroke Raymond Floyd
Mike Hulbert 90,000 500,000
1985 Fuzzy Zoeller United States 275 −9 2 strokes Tom Watson 90,000 500,000
Bay Hill Classic
1984 Gary Koch (2) United States 272 −12 Playoff George Burns 72,000 400,000
1983 Mike Nicolette United States 283 −1 Playoff Greg Norman 63,000 350,000
1982 Tom Kite United States 278 −6 Playoff Jack Nicklaus
Denis Watson 54,000 300,000
1981 Andy Bean United States 266 −18 7 strokes Tom Watson 54,000 300,000
1980 Dave Eichelberger United States 279 −5 3 strokes Leonard Thompson 54,000 300,000
Bay Hill Citrus Classic
1979 Bob Byman United States 278 −6 Playoff John Schroeder 45,000 250,000
Florida Citrus Open
1978 Mac McLendon United States 271 −17 2 strokes David Graham 40,000 200,000
1977 Gary Koch United States 274 −14 2 strokes Dale Hayes
Joe Inman 40,000 200,000
1976 Hale Irwin United States 270 −18 Playoff Kermit Zarley 40,000 200,000
1975 Lee Trevino United States 276 −12 1 stroke Hale Irwin 40,000 200,000
1974 Jerry Heard (2) United States 273 −15 3 strokes Homero Blancas
Jim Jamieson 30,000 150,000
1973 Buddy Allin United States 265 −23 8 strokes Charles Coody 30,000 150,000
1972 Jerry Heard United States 276 −12 2 strokes Bobby Mitchell 30,000 150,000
Florida Citrus Invitational
1971 Arnold Palmer United States 270 −18 1 stroke Julius Boros 30,000 150,000
1970 Bob Lunn United States 271 −17 1 stroke Arnold Palmer
Bob Stanton 30,000 150,000
Florida Citrus Open Invitational
1969 Ken Still United States 278 −10 1 stroke Miller Barber 23,000 115,000
1968 Dan Sikes United States 274 −14 1 stroke Tom Weiskopf 23,000 115,000
1967 Julius Boros United States 274 −10 1 stroke George Knudson
Arnold Palmer 23,000 115,000
1966 Lionel Hebert United States 279 −5 2 strokes Charles Coody
Dick Lytle
Jack Nicklaus 21,000 110,000
* rain-shortened to 54 holes
Note: Green highlight indicates scoring records.
Sources[6][7]
Multiple winners[edit]
Seven men have won this tournament more than once through 2018.
8 wins
Tiger Woods: 2000, 2001, 2002, 2003, 2008, 2009, 2012, 2013
2 wins
Jerry Heard: 1972, 1974
Gary Koch: 1977, 1984
Tom Kite: 1982, 1989
Loren Roberts: 1994, 1995
Ernie Els: 1998, 2010
Matt Every: 2014, 2015
Tournament highlights[edit]
1966: Lionel Hebert wins the inaugural version of the tournament. He wins by two shots over Jack Nicklaus, Charles Coody, and Dick Lytle.[8]
1968: Dan Sikes breaks out of a 5-way logjam to win by one shot over Tom Weiskopf. At the end of 54 holes, Sikes had been tied for the lead with Jack Nicklaus, Bruce Devlin, Miller Barber, and Bob Charles. Officials said this was the first time there had ever been a five-way tie for the lead after 54 holes at a PGA event.[9]
1971: Arnold Palmer wins the event eight years before he becomes its host. He beats Julius Boros by one shot.[10]
1973: Vietnam War veteran Buddy Allin shoots a tournament record 23 under par to breeze to an eight shot victory over Charles Coody.[11]
1974: Jerry Heard becomes the tournament's first two-time winner. He beats Homero Blancas and Jim Jamieson by two shots.[12]
1976: Early on a Monday morning, Hale Irwin defeats Kermit Zarley on the sixth hole of a sudden death playoff after play was suspended due to darkness on Sunday.[13] While speaking to the press on Sunday evening, Irwin blamed NBC Sports for there not being enough time to finish the playoff.[14]
1979: Bob Byman wins the first edition of the tournament to be played at Bay Hill. He defeats John Schroeder on the second hole of a sudden death playoff.[15]
1980: Dave Eichelberger wins by three shots over Leonard Thompson.[16] The temperatures were so cold that Eichelberger wore panty hose during the final round.[17]
1982: Tom Kite chips in for birdie on the first hole of a sudden death playoff to defeat Jack Nicklaus and Denis Watson.[18]
1984: Gary Koch shoots a final round 63 before defeating George Burns on the second hole of a sudden death playoff. Koch is the only champion in the tournament's history to win both at Rio Pinar and Bay Hill.[19]
1985: Coming off back surgery less than six months previously, Fuzzy Zoeller wins at Bay Hill. He finishes two shots ahead of Tom Watson.[20]
1987: Payne Stewart, who owned a home just off Bay Hill's 12th tee, notches his third career PGA Tour title. He beats David Frost by three shots.[21]
1989: Tom Kite wins for a second time at Bay Hill by defeating Davis Love III on the second hole of a sudden death playoff. Before the playoff took place, both Kite and Love made double bogey on the tournament's 72nd hole.[22]
1990: Robert Gamez holes a 7-iron on the 72nd hole for an eagle two allowing him to win by one shot over Greg Norman.[23]
1992: Fred Couples wins by nine shots over Gene Sauers. With his win, Couples becomes the #1 ranked player in the world.[24]
1995: Loren Roberts becomes the first returning champion to successfully defend his title. He beats Brad Faxon by two shots.[25]
1996: Paul Goydos wins for the first time on the PGA Tour. He beats Jeff Maggert by one shot and Tom Purtzer by two.[26] During the tournament's second round, Purtzer incurred a two-shot penalty by playing the wrong ball.
1998: During the tournament's final round, John Daly hits six balls in the water on the sixth hole. He finishes the hole with a final score of 18.[27]
2000: Tiger Woods wins at Bay Hill for the first time. He beats Davis Love III by four shots.[28]
2003: Tiger Woods becomes the first golfer since Gene Sarazen at the 1930 Miami Open to win the same tournament in four consecutive years. He wins by 11 shots over Kirk Triplett, Stewart Cink, Kenny Perry, and Brad Faxon.[29]
2005: Kenny Perry wins by two shots over Vijay Singh and Graeme McDowell. Perry and Singh were tied for the lead until Singh made double bogey at the 72nd hole.[30]
2008: Tiger Woods sinks a 25-foot birdie putt at the 72nd hole to defeat Bart Bryant by one shot.[31] It's Woods fifth Bay Hill triumph in addition to his winning the fifth consecutive tournament he had played in.
2009: Tiger Woods wins at Bay Hill for the 2nd straight year and sixth time overall. He birdies the 72nd hole to defeat Sean O'Hair by one shot.[32]
2012: Tiger Woods wins the Arnold Palmer Invitational for the seventh time, ending a winless streak on the PGA Tour dating back 27 events to September 13, 2009.[33]
2013: Tiger Woods wins for a record-tying eighth time at the Arnold Palmer Invitational while holing three eagles during the week, the first time a player has accomplished the feat since 2001; he ascends to the number 1 ranking for the first time since October 2010.[34]
2014: With world number one Woods out of the tournament, the focus was on world number two Adam Scott. Scott led the first three rounds, but struggled in the fourth round, finishing third behind Keegan Bradley and first-time PGA Tour winner Matt Every.
2015: Matt Every holed an 18-foot birdie putt on the 72nd hole to beat Henrik Stenson by one shot and become the third golfer to defend his title at the Arnold Palmer Invitational. In the third round, Daniel Berger recorded a double eagle at the par-5 6th hole, the first since the tournament moved to Bay Hill in 1979. Zach Johnson repeated the feat in the final round on the par-5 16th.[35][36]
References[edit]
Jump up ^ "MasterCard Extends Presenting Sponsorship of Arnold Palmer Invitational". MasterCard.com (Press release). March 21, 2012. Retrieved March 26, 2012.
Jump up ^ "MasterCard Extends Sponsorship". ArnoldPalmerInvitational.com. March 21, 2012. Archived from the original on April 7, 2012. Retrieved March 26, 2012.
Jump up ^ "Boost to Arnie and Jack tourneys". ESPN. Associated Press. June 3, 2014.
Jump up ^ "2015–16 PGA Tour Player Handbook & Tournament Regulations" (PDF). October 5, 2015. Archived from the original (PDF) on April 12, 2016.
Jump up ^ "Course: Bay Hill Club". PGA Tour. 2013. Retrieved March 27, 2013.
Jump up ^ Arnold Palmer Invitational - Winners - at www.pgatour.com
Jump up ^ Arnold Palmer Invitational - Winners Archived 2011-07-16 at the Wayback Machine. - at www.golfobserver.com
Jump up ^ Hebert Discards Remedy, Wins Florida Citrus Open
Jump up ^ Dan Sikes wins Citrus Open
Jump up ^ Palmer Cops Citrus Open
Jump up ^ Allin Citrus Champ
Jump up ^ Jerry Heard regains winning touch, takes Citrus Open on 273 total
Jump up ^ Citrus Open playoff won by Hale Irwin
Jump up ^ Irwin Raps TV For Late Start
Jump up ^ Byman steps up in Citrus
Jump up ^ Eichelberger wins chilly Bay Hill
Jump up ^ Golfers required panty hose
Jump up ^ Kite wins Bay Hill Golf in three-man playoff
Jump up ^ Gary Koch wins Bay Hill playoff
Jump up ^ Fuzzy Zoeller wins Bay Hill Classic
Jump up ^ Stewart wins Bay Hill by 3
Jump up ^ Kite catches Love and wins playoff
Jump up ^ Spectacular eagle wins for Gamez
Jump up ^ Sizzling Couples coasts by 9 shots in Nestle laugher
Jump up ^ Roberts and Bay Hill Links Seem Made for Each Other
Jump up ^ Goydos fires 67 to capture Bay Hill
Jump up ^ Six In Lake Give Daly an 18
Jump up ^ Woods Triumphs Again, Leaving Love in Awe
Jump up ^ Ailing Woods wins 4th straight Bay Hill by 11 strokes
Jump up ^ Perry Wins Bay Hill After Singh Suffers Rocky Finish
Jump up ^ Tiger birdies 18 for title
Jump up ^ Golf-Woods overhauls O'Hair for comeback win at Bay Hill
Jump up ^ Donegan, Lawrence (March 26, 2012). "Tiger Woods ends PGA Tour drought with Arnold Palmer Invitational win". The Guardian. Retrieved March 28, 2013.
Jump up ^ Schmitz, Brian (March 26, 2013). "Tiger Woods is back at No. 1 after winning Arnold Palmer Invitational". Los Angeles Times. Retrieved March 28, 2013.
Jump up ^ "Matt Every wins again at Bay Hill". ESPN.com. Retrieved March 22, 2015.
Jump up ^ "Daniel Berger makes 2 on par 5". ESPN.com. Retrieved March 22, 2015.
External links[edit]
Official website
Coverage on the PGA Tour's official site
Bay Hill Club and Lodge
Rio Pinar Country Club
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