About this sample
About this sample
Words: 1283 |
7 min read
Published: Mar 18, 2021
Words: 1283|Pages: 3|7 min read
The dividing life of a cell is called cell cycle that includes growth, doubling genetic material and dividing into new cells. Cell cycle has 2 subgroups: interphase and mitosis. Interphase refers to ‘’getting ready to divide’’. Interphase has 3 subphases that are; G1, S, and G2. On the other hand, there is G0 phase called quiescent state. At G0 phase cells do not have any division process, cells only maintain their living process without growth. Mitosis represents the cell division that has 5 subphases; prophase, metaphase, anaphase, telophase, and cytokinesis where cytoplasmic division occurs. External signals have an effect on cell to decide entering the cell cycle process. Mitogenic growth factors trigger the cells for active growth and cell division if they are presence sufficient concentration in the cell environment. But if they are not enough concentration in the environment, cell remains G0 phase. The cell maintains at G0 when growth inhibitory factors are entity such as TGF-β. Tyrosine kinase receptors, G-coupled receptors, integrins, and nutrient status can be given as examples for other external signals. As mentioned above G1 is one of the interphase’s subphases in which cell decides about growth or quiescence with differentiation. Cell growth occur and biosynthesis increases at G1 phase. In mammalian cell, G1 takes 6 to8 hours. DNA duplication takes place at S phase. Centrosome also duplicates itself and histone protein amount increases.
Spindle apparatus can be seen at G2 phase. After interphase section ends cells go mitosis where nuclear and cytoplasmic division occur. Chromosome condensation, centrosome localization, and disappearance of nucleolus are located in prophase. During metaphase, chromosomes align metaphase plate, nuclear envelope disappears, microtubules attach chromosomes at kinetochore that interacts with centromere where two sister chromatids are hold together. Sister chromatids are pulling opposite poles of cell during anaphase. While telophase, chromatids are decondensed and nuclear envelope forms for each chromatid sets.
After all these steps occur, cytoplasmic division called cytokinesis begins. As can be understood, cell cycle process is long and toilsome. Also, different diseases show up including cancer if there is problem at any stage of cell cycle. Therefore, cells have checkpoints where the cell cycle is controlled. These check points are named as G1 checkpoint, G2 checkpoint, and M checkpoint. At G1 checkpoint, DNA integrity, size, molecular signal, and nutrients are checked. If there is no problem, the cell undergoes S phase. In contrast, if there is a problem cell undergoes G0 phase. DNA integrity and appropriate DNA replication are checked at G2 phase. The cell activates repair system when there is a challenge. If this challenge cannot be repairable, cell undergoes apoptosis or programmed cell death. This checkpoint is crucial to prevent cancer formation. M checkpoint controls chromosome- spindle attachment at metaphase plate. As mentioned above, the cell makes a decision about growth and quiescence. This decision is related to external signals. The anti-mitogenic factors such as TGF-β which has growth-inhibitory effect.
On the other hand, mitogenic growth factors induce cell to grow. At restriction point, which is located late G2, the cell decides to move G0 or S phase. Cell cycle process is regulated by different genes and proteins. Cyclin, cyclin dependent kinases (CDK), CDK inhibitors, apoptosis promoting complex/cyclosome (APC/C), p53 and pRb are most common research areas when the subject is cell cycle. Cyclin dependent kinases that are inactive on their own, are responsible activation of targets via phosphorylation while they are active with cyclins. The CDKs are participant of serine/threonine kinases that have an interaction with growth factor receptor and with nonreceptor kinase molecule. Cyclins have an important role for catalytic activation and recognition ability of CDKs during binding process of their protein substrate. At G1 phase, CDK4 and CDK6 are activated by D-type cyclins (D1, D2, and D3). When R point in late G2 is passed, E-type cyclins interacts with CDK2. This process allows cell to undergo S phase by phosphorylation of appropriate protein substrates. CDK2 associates with A-type cyclins (dissociates E-type cyclins) at S phase and allows to progress S phase. A-type cyclins associate with CDC2 or CDK1 later in S phase. When cell undergoes G2 phase, CDC2 makes a deal with B-type cyclins that trigger mitosis events such as prophase, metaphase, anaphase, and telophase. The external mitogens such as Wnts via β-catenin and Tcf/Lef transcription factor, cytokine via STAT, and various ligands via NF-KB increase cyclinD1 which lead to cell cycle. CDK inhibitors (CDKI) are important proteins that have negative effect on cell cycle. INK4 (inhibitors of CDK4) are targeting CDK4 and CDK6 without any effect on CDC2 and CDK4. INK4 inhibitors are p16INK4a, p15INK4b, p18INK4c, p19INK4d. All the other cyclin-CDK complexes (E-CDK2, A-CDK2, A-CDC2, B-CDC2) are inhibited by p21Cip1 (or named as p21Waf1), p27Kip1, and p57Kip2. When TGF-β is presence in the environment of the cell, that triggers p15INK4b that blocks the cyclin D-CDK4/6 complexes. Because of that, cell does not reach R point in late G2 without cyclin D/CDK4/6. p21Cip1 used during the damage repair system inhibits cyclin E-CDK2 complexes until DNA damage is repaired. Surprisingly, there is a different process found in p21Cip1 and p27Kip1. They have role in cyclin E-CDK2 inhibition on the other hand they stimuli cyclin D-CDK4/6 complex formation. Binding M cyclin to CDKs promotes cell to undergo mitosis.
The other protein is anaphase promoting complex/cyclosome (APC/C). This complex causes degradation of M cyclin and destruction of cohesin protein that holds sister chromatids together, so APC/C allows separation of chromotids in anaphase through opposite site. APC/C has different work process from CDKs. It adds ubiquitin to its target that causes degradation of protein by proteasome. The pathway of degradation of cohesin starts ubiquitin addition to securin which binds separase enzyme to inactivate the separase. When securin is ubiquitinated that is destroyed by proteasome and separase becomes active. Active separase takes role in degradation of cohesin that results in sister chromatids separation. p53 is another protein known as tumor suppressor. p53 triggers formation of CDKIs, that destroy cyclin/CDK complexes, when there is a DNA damage. Also, it activates DNA repair enzymes. If this damage is not fixable, P53 act as stimuli for programmed cell death. pRb works as tumor suppressor, too. pRb binds E2F transcription factor, whose role is effect cell to enter S phase. When mitogenic signals activates G1 cyclin formation, it suppresses pRb and causes releasing of E2F from pRb. Activated E2F allows cell to enter S phase. Any mutation on p53 or pRb gives opportunity to cell to divide limitlessly as tumor.
In addition, any mutation on G1 cyclin gene (CCNG1) that consequence increase of expression, causes MDM2 protein activation. MDM2 makes p53 to target for proteasome by addition of ubiquitin. When p53 is degraded cell cycle arrest could not occur, thus tumor formation is observed. As a conclusion, cell cycle is a process that includes cell growth and division. Different proteins have active roles in this process to continue the cell cycle and also, cell cycle requires regulation to prevent tumor formation.
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