CELL Cycle - Lecture Notes PDF

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THE CELL CYCLE The cell cycle of the eukaryotic cell can be divided into 4 stage process with two major phases the interphase and the mitotic phase (M). In the interphase there are three phases, and this is when the cell prepares for division and the stages are G 1, S and G2 phase, followed by this the M phase occur (Li & Burridge, 2019). The cellular events which occur in each of the interphase stages are: - G1 Phase: This phase is also known as the first gap phase, and in this stage the cell grows physically increasing the size, the cellular components are copied such as the organelles, and the molecular building blocks which are needed for later steps are made (Li & Burridge, 2019). - S Phase: In this phase the cell synthesis a complete copy of the DNA within the nucleus known as the DNA replication, thus each of the 46 chromosomes which are 23 pairs are replicated by the cell. The microtubule organizing structures known as the centrosome is also duplicated, which is used in the later phase to separate the DNA (Li & Burridge, 2019). - G2 Phase: This phase is also known as the second gap phase, and in this phase the cell grows further. The organelles and the proteins are developed in this stage for the cells division. This phase ends when the mitosis begins (Li & Burridge, 2019). After the interface the mitotic (M) phase occurs. There are two distinct division related processes in this phase and they are: Mitosis and cytokinesis. In mitosis, the DNA of cell condenses and is pulled apart by the mitotic spindle (Kao et al, 2015). The mitotic then happens in four stages: - Prophase: Mitosis begins with this stage, in which the cell breaks down some structure and build to setting stages for the division of the chromosomes. The chromosomes also start to condense and the mitotic spindle beings to form, and the spindle grows between the centrosomes as they move apart. In this stage the nucleolus, a part of the nucleus disappears. This is a sign of the nucleus getting ready to break down (Kao et al, 2015).. - Prometaphase: This stage is also known as late prophase. In this stage the chromosome become more condensed. The nucleus envelop also breaks down in this stage releasing the chromosomes. To add on, the mitotic spindle grows more, and some microtubules bind to the chromosomes at kinetochore (Kao et al, 2015).. - Metaphase: In this phase all the chromosomes align at the metaphase plate, which is the middle of the cell. The kinetochores of each chromosome are also attached to the microtubules (Kao et al, 2015). - Anaphase: The protein which holds the sister chromatid is broken resulting in each pair of the chromosomes to be pulled towards the opposite ends of the cell. Also, the microtubules which are not attached to the chromosome elongate causing to push apart resulting the cell to be longer as the poles separates. The motor proteins are the proteins which drives these processes (Kao et al, 2015). - Telophase: In this stage the mitotic spindle is brown and two nuclei forms with one nuclei for each chromosomes sets. The chromosomes also begin to decondense, and the nucleoli and nuclear membrane reappears (Kao et al, 2015). Then happens cytokinesis, in which the cytoplasm of the cell is split into two new cells, which are the two identical daughter cell. However, the cytokines occur differently in both animal and plants cells because in animal cells the contractile ring a brand of cytoskeletal fibres contract inwards and pinches the cell, which is known as contractile cytokinesis. While

in plant cells the cells are surrounded by a rigid cells wall and the internal pressure is high resulting in the cells to divide by forming a new structure known as cell plate in the middle of the cell. This marks the end of the cell cycle (Kao et al, 2015). However, after completing the cell cycle, the cell type of the daughter cell decide the next steps. Some types of c ell divide rapidly, resulting in the daughter cell undergoing another cell division round (Li & Burridge, 2019). While other types of cell divides rapidly or not at al. These cells exist in the G1 phase and enter the G0 phase which is the resting state. Cells in the G0 phase is not preparing to divide instead performs its function. Some cells in G 0 are in a permanent state while other may re-start division if the signals are right (Li & Burridge, 2019). To add on, during cell cycle there are also checkpoints or regulations at different point which detect if there is damaged DNA on the cell, and if there are the cell cycle regulators ensure that they do not replicate and divide, thus regulators control the cell cycle (Hu, 1994). One of the core cell cycle regulators are Cyclins. They are a group of related protein and there are 4 basic types in most eukaryotic such as (Hu, 1994): - G1 Cyclins - G1 / S Cyclins - S Cyclins - M Cyclins Each of these cyclins are associated with a particular phase transition or a set of phases in the cell cycle. Moreover, for the cell cycle to progress the cyclin must activate or inactive various target protein within the cell, and this is done by the cyclin binding with the enzyme Cdks which activates the Cdk (Hainaut et al, 2005). The Cdks does this by phosphorylating the specific target proteins. Therefore, when the cyclin and Cdk binds it activates the CDK kinase and the Cdk is also directed to specific set of targeted proteins within the cell cycle, and the activity of these protein are needed for cell cycle to progress and be completed (Hainaut et al, 2005). To add on, eukaryotes have multiple cyclins and in cell cycle each Cdk is paired with only a specific cyclin and these are (Hainaut et al, 2005); o CDK1 & CDK2 - Cyclin A,B,D,E o CDK4 & CDK6 – Cyclin D Moreover, a transcription factor known as the P53 acts as a mechanism for proof reading which is a signalling mechanism for the apoptosis. The P53 detects the DNA damage in the cell cycle during the synthesis phase and send signals which indicate the severity of the damage to repair the damage which the p53R2 protein caused (Yan et al, 2021). P53 is also referred to as a tumour suppressor which regulate the cell cycle and cell division and the transcription factor is coded by the gene TP53 (Elmore, 2007). In normal eukaryotic condition the p53 level are low cause of the degradation by ubiquitylation of the proteasomal which is associated with the MDMD2, and when a damage of DNA is detected a release of p53 is trigged resulting the P53 levels to rise in the nucleus of the cell through the chemical modification of phosphorylation and acetylation (Elmore, 2007). As the p53 level increases the dissociation of MDM2 from P53 occurs. The transactivation on the p53 acts on the target genes resulting in cell cycle to be paused which is known as the cell cycle arrets or the apoptosis (Elmore, 2007). Therefore, the apoptosis causes the damage on the DNA to be repaired if it is not too severe, after which the cell is re-transitioned back into the cell cycle. However, the cell will be eliminated by the P53 through the function known as pro-apoptotic if the damage is unrepairable (Elmore, 2007). Moreover, the P53 promotes the cell arrest by

two apoptotic pathway, the extrinsic in which the conditions in the extracellular environment of the cell determines the cell arrest or the intrinsic which is resulted from stress by an injury within the cell (Elmore, 2007). Therefore, these two pathways which is stimulated by the p53 in addition to the activated protein cause cell arrest or apoptotic (Elmore, 2007). Finally, the tumour suppressor gene is a type of gene which produces a protein known as the tumour suppressor and the aim of this protein is to control the cell growth. However, mutations in this gene can lead to cancer (Yan et al, 2021). While an oncogene is a mutated gene which contribute to the cancer development and the unmutated state of this oncogenes are known as proto-oncogenes and it plays a major role in the cell division regulation (Yan et al, 2021). Moreover, the P53 gene was identifies aa oncogene originally however ten years after it was conformed to be a tumour suppressor gene (Yan et al, 2021). This is because the P53 is inactivated directly in half of the tumours because of the mutation in the P53 gene and it is inactivated indirectly to the viral protein through binding which causes the genes of the products which interact with the P53 to alter or transmit information from or to the p53 (Yan et al, 2021). Therefore, with the evidence of various research as stated above it can be stated that p53 gene is a tumour suppressor gene, and the p53 is a tumour suppressor protein (Yan et al, 2021)....