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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 the restriction point or START and is regulated by G1/S cyclins, which cause transition from G1 to S phase. Passage through the G1 check point commits the cell to division.
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
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Science Creative Quarterly's overview of the cell cycle
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Financial institution
From Wikipedia, the free encyclopedia
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Financial institutions are corporations which provide services as intermediaries of financial markets. Broadly speaking, there are three major types of financial institutions:[1][2]
Depository institutions – deposit-taking institutions that accept and manage deposits and make loans, including banks, building societies, credit unions, trust companies, and mortgage loan companies;
Contractual institutions – insurance companies and pension funds
Investment institutions – investment banks, underwriters, brokerage firms.
Some experts see a trend toward homogenisation of financial institutions, meaning a tendency to invest in similar areas and have similar business strategies. A consequence of this might be fewer banks serving specific target groups, and small-scale producers may be under-served.[3]
Contents
[hide]
1 Standard settlement instructions
2 Regulation
3 See also
4 References
Standard settlement instructions[edit]
Standard Settlement Instructions (SSIs) are the agreements between two financial institutions which fix the receiving agents of each counterparty in ordinary trades of some type. These agreements allow traders to make faster trades since the time used to settle the receiving agents is conserved. Limiting the trader to an SSI also lowers the likelihood of a fraud. SSIs are used by financial institutions to facilitate fast and accurate cross-border payments.
Regulation[edit]
Financial institutions in most countries operate in a heavily regulated environment because they are critical parts of countries' economies, due to economies' dependence on them to grow the money supply via fractional reserve lending. Regulatory structures differ in each country, but typically involve prudential regulation as well as consumer protection and market stability. Some countries have one consolidated agency that regulates all financial institutions while others have separate agencies for different types of institutions such as banks, insurance companies and brokers.
Countries that have separate agencies include the United States, where the key governing bodies are the Federal Financial Institutions Examination Council (FFIEC), Office of the Comptroller of the Currency - National Banks, Federal Deposit Insurance Corporation (FDIC) State "non-member" banks, National Credit Union Administration (NCUA) - Credit Unions, Federal Reserve (Fed) - "member" Banks, Office of Thrift Supervision - National Savings & Loan Association, State governments each often regulate and charter financial institutions.
Countries that have one consolidated financial regulator include: Norway with the Financial Supervisory Authority of Norway, Germany with Federal Financial Supervisory Authority and Russia with Central Bank of Russia.
See also[edit]
Bank
Consumer Credit Act 1974 (UK law)
Credit union
Financial economics
Fractional-reserve banking
International financial institutions
List of financial regulatory authorities by country
Non-bank financial institution
Savings and loan association
Society for Worldwide Interbank Financial Telecommunication
References[edit]
Jump up ^ Siklos, Pierre (2001). Money, Banking, and Financial Institutions: Canada in the Global Environment. Toronto: McGraw-Hill Ryerson. p. 40. ISBN 0-07-087158-2.
Jump up ^ Robert E. Wright and Vincenzo Quadrini. Money and Banking: Chapter 2 Section 5: Financial Intermediaries.[1] Accessed July 24, 2012
Jump up ^ Jayati Gosh (January 2013). "Too much of the same". D+C Development and Cooperation/ dandc.eu.
Authority control
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'Til Summer Comes Around
From Wikipedia, the free encyclopedia
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"'Til Summer Comes Around"
Single by Keith Urban
from the album Defying Gravity
Released
November 23, 2009 (2009-11-23)
Format
Music download
Recorded
2009
Genre
Country
Length
5:31 (album version)
3:53 (radio edit)
Label
Capitol Nashville
Songwriter(s)
Monty Powell, Keith Urban
Producer(s)
Dann Huff, Keith Urban
Keith Urban singles chronology
"Only You Can Love Me This Way"
(2009) "'Til Summer Comes Around"
(2009) "I'm In"
(2010)
"Only You Can Love Me This Way"
(2009) "'Til Summer Comes Around"
(2009) "I'm In"
(2010)
"'Til Summer Comes Around" is a song co-written and recorded by Australian country music singer Keith Urban. It was released in November 2009 as the fourth single from his album Defying Gravity. The song peaked at number 3 on the US Billboard Hot Country Songs chart. Urban wrote this song with Monty Powell.
Contents
[hide]
1 Content
2 Music video
3 Critical reception
4 Chart performance
4.1 Year-end charts
5 Awards
6 References
Content[edit]
The narrator compares a quiet boardwalk in the wintertime to something "empty as [his] broken heart," remembering the times that he and his lover had at the carnival rides there while the boardwalk was open in the summertime. As the song progresses, it is revealed that he has remained in the town for several years, waiting for her to return, as promised, in the summer.[1] It is accompanied mostly by electric guitar and organ.[2]
Music video[edit]
The music video, directed by Noble Jones, was released on January 12, 2010. It won the Male Video of the Year Award at the 2010 CMT Music Awards. It debuted on CMT's Top Twenty Countdown at number 12 on the week of January 22, 2010, and has since reached number 3. It was filmed in Santa Monica, CA.
Critical reception[edit]
Thom Jurek of Allmusic referred to the song as "haunting, nocturnal, and dreamily textured" in his review of the album.[3] Bobby Peacock of Roughstock said that it was "more substantial" than the album's other three singles and "a standout even among [Urban’s] many great ballads."[2] Chris Neal of Country Weekly gave it four-and-a-half stars out of five, saying that "[t]he words paint a vivid picture of a setting that perfectly mirrors the narrator's emotional state" and calling it "one of [Urban’s] best [singles] to date."[1]
Chart performance[edit]
"'Til Summer Comes Around" debuted at number 41 on the Billboard Hot Country Songs charts dated November 28, 2009. Before the song's release, a Keith Urban fan blog called Urban Country Blog had started a petition to release the song as a single.[1] It also debuted at number 92 on the Billboard Hot 100 and has peaked at number 58. It reached a peak of number three on the Hot Country Songs charts in 2010.
Chart (2009–2010)
Peak
position
Canada (Canadian Hot 100)[4] 74
US Billboard Hot 100[5] 58
US Hot Country Songs (Billboard)[6] 3
Year-end charts[edit]
Chart (2010)
Position
US Country Songs (Billboard)[7] 13
Awards[edit]
The song won the 2011 Grammy Award for Best Male Country Vocal Performance on February 13, 2011.[8]
References[edit]
^ Jump up to: a b c Neal, Chris (2009-12-14). "Reviews — Singles". Country Weekly. 16 (44): 54. ISSN 1074-3235.
^ Jump up to: a b Peacock, Bobby (2009-11-19). "Keith Urban — "'Til Summer Comes Around"". Roughstock. Archived from the original on 23 November 2009. Retrieved 20 November 2009.
Jump up ^ Jurek, Thom. "Defying Gravity review". Allmusic. Retrieved 2009-11-20.
Jump up ^ "Keith Urban Chart History (Canadian Hot 100)". Billboard. Retrieved April 10, 2011.
Jump up ^ "Keith Urban Chart History (Hot 100)". Billboard. Retrieved April 10, 2011.
Jump up ^ "Keith Urban Chart History (Hot Country Songs)". Billboard. Retrieved April 10, 2011.
Jump up ^ "Best of 2010: Country Songs". Billboard. Prometheus Global Media. 2010. Archived from the original on 11 December 2010. Retrieved December 13, 2010.
Jump up ^ Tucker, Ken (13 February 2011). "Lady Antebellum Tops Grammys". Country Weekly. Archived from the original on 17 February 2011. Retrieved 14 February 2011.
hide
v
t
e
Keith Urban singles
Keith Urban (1991)
"Only You"
"I Never Work on a Sunday"
"Arms of Mary"
"The River"
Keith Urban (1999)
"It's a Love Thing"
"Your Everything"
"But for the Grace of God"
"Where the Blacktop Ends"
Golden Road
"Somebody Like You"
"Raining on Sunday"
"Who Wouldn't Wanna Be Me"
"You'll Think of Me"
Be Here
"Days Go By"
"You're My Better Half"
"Making Memories of Us"
"Better Life"
"Tonight I Wanna Cry"
Love, Pain & the Whole Crazy Thing
"Once in a Lifetime"
"Stupid Boy"
"I Told You So"
"Everybody"
Greatest Hits: 19 Kids
"You Look Good in My Shirt"
Defying Gravity
"Sweet Thing"
"Kiss a Girl"
"Only You Can Love Me This Way"
"'Til Summer Comes Around"
"I'm In"
Get Closer
"Put You in a Song"
"Without You"
"Long Hot Summer"
"You Gonna Fly"
Act of Valor: The Album
"For You"
Fuse
"Little Bit of Everything"
"Shame"
"We Were Us" (with Miranda Lambert)
"Cop Car"
"Somewhere in My Car"
"Raise 'Em Up" (with Eric Church)
Ripcord
"John Cougar, John Deere, John 3:16"
"Break on Me"
"Wasted Time"
"Blue Ain't Your Color"
"The Fighter" (with Carrie Underwood)
Graffiti U
"Female"
"Parallel Line"
"Coming Home" (with Julia Michaels)
Guest singles
"America the Beautiful"
"The Twelfth of Never" (with Dolly Parton)
"Funky Tonight" (with The John Butler Trio)
"In God's Hands" (with Nelly Furtado)
"Start a Band" (with Brad Paisley)
"Blue Sky" (with Emily West)
"Lean on Me" (with Sheryl Crow and Kid Rock)
Related articles
"Highway Don't Care" (with Tim McGraw and Taylor Swift)
Retrieved from "https://en.wikipedia.org/w/index.php?title=%27Til_Summer_Comes_Around&oldid=849272515"
Categories:
Keith Urban songs
2009 singles
Songs written by Monty Powell
Songs written by Keith Urban
Song recordings produced by Dann Huff
Grammy Award for Best Male Country Vocal Performance winners
Capitol Records Nashville singles
2009 songs
Country ballads
Hidden categories:
Articles with hAudio microformats
Singlechart usages for Canada
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Singlechart usages for Billboardhot100
Singlechart usages for Billboardcountrysongs
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This page was last edited on 7 July 2018, at 20:26 (UTC).
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization.
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