Detailed Overview of the Cell Cycle for Molecular Biology

This report provides a comprehensive overview of the cell cycle, detailing the various phases including G1, S, G2, mitosis, and cytokinesis. It explores the key controllers, such as cyclin-dependent kinases (CDKs) and cyclins, and their roles in regulating the cycle. The report also discusses cyclin expression, activation of cyclin-CDK, and the switch-like activation mechanism. Furthermore, it delves into the factors determining when a cell should divide, including mitogens and anti-mitogens, and their impact on cell division initiation. The report also discusses cell growth, cell division, and the role of mTOR. Finally, the report touches upon cell cycle checkpoints that ensure proper progression. The report is based on a variety of research articles and online sources.

Overview of cell cycle
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Table of Contents
INTRODUCTION...........................................................................................................................3
REFERENCES................................................................................................................................4
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INTRODUCTION
Human body is made of large number of cells. There are trillion of cells that perform
different functions. It has been summarised that cell division produce two cells from one single
cell. The cell consists of same chromosomes and other protein which enable them to survive in
human body.
Cell cycle phases
It has been found that there are 5 phases of cell development that is pro, prometa, meta,
anaphase and telophase. G1 is growth phase in which cell size increases. Then, in S phase DNA
replication occur. However, in G2 phase in which centrosomes duplicates. They set spindle
which enable in separating of chromosomes (Cai, and et.al., 2018). In mitosis phase there is
change in cell structure. Here, spindle form microtube from centrosomes and chromosomes is
aligned within centre of spindle. Moreover, in last stage the chromosomes migrate to opposite
cell side. The last stage is known as cytokinesis in which cell constrict in middle of cell
membrane. Thus, it results in dividing cell into two parts. G0 can also be stage in it where cell
exist cell cycle.
Cell cycle controllers
It is necessary that cell cycle goes smoothly in systematic way. Here, DNA replication
occurs which enable in separating of chromosomes. However, it must occur before cytokinesis.
Thus, in this there is centralise controller which ensure that all process is done in proper way.
Basically, controller is made of two proteins that are cyclin dependent kinase and cyclin. The
function of CDK is to phosphorylate protein whereas cyclin function is to regulate activity of
CDK.
Cyclin expression and cell cycle phase
It has been stated that there are various types of cyclin that occur in different phase. Thus,
if there is occur of expressed cyclin then it relates with CDK. So, various cyclin are E, S, M and
APC. In S cyclin activate DNA replication, in M phase spindle is attached to chromosomes. And
in last APC it destroys all cyclin and separate chromatids. Basically, cyclin proceed in wave in
cell cycle. Thus, on basis of it cyclin got their names. Moreover, cyclin CDK get into one phase
and then it activates cyclin expression in next one (Godard, and Heisenberg, 2019). Therefore,
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it enables in proceeding in wave like. But on other hand, it is found that CDK is same within
entire cell cycle.
Activation of cyclin- CDK
It can be concluded that this process consists of 3 stages which are as follows
In first CDK is bind to cyclin. So, it covers 100 amino acid domain in CDK that is known as
cyclin box. So, it activates opening of kinase pocket.
The second is medicate of CDK by kinases. CAK’s phosphate result in opening of substrate
binding site. It gets activate in most cells.
The last step is removing of phosphate from CDK. In this Wee1 kinase add phosphate in ATP
that led to reducing kinase activity. So, CDK bound and phosphorylated get inactivated by
Wee1. In addition, Cdc25 remove phosphate from CDK. However, activating of cyclin CDK get
regulated with help of positive feedback. In this active cyclin generate more Cdc25. Furthermore,
CDK inhibit Wee1 that decrease ability to add phosphate to CDK.
Switch like activation of cyclin CDK
It is found that positive feedback activates cyclin CDK in each cell. So, it plays vital role
in activating cyclin CDK. This can be said that in cell cycle CDK is same but cyclin increase
before cell cycle. Thus, when signal activate in cyclin the protein in it gradually increases. This
all happens when there is no positive feedback (Gudipaty, and et.al., 2017).
But on contrary there is drawback as well of increase in cyclin CDK. First is that this
event starts at different time which can led to high increase in cyclin CDK. Another is that cyclin
CDK can be reverse as signal activated in it can be removed. Therefore, it will result in
decreasing amount of cyclin CDK. However, positive feedback helps in overcoming these
limitations by activating cyclin CDK. This starts before next stage of cell cycle. It is found that
cyclin start CDK but they are not active. This is because of no presence of phosphate that is
Wee1. Hence, it leads to forming of large cell. When cell is ready to go in next stage Ccd25 is
activated. This remove phosphate on CDK. Hence, with help of positive feedback CDK active
more cyclin. Therefore, CDK is independent as it maintains own activity with help of positive
feedback. Besides that, it is analysed that cyclin CDK is not turned off automatically. But rather
cell target cyclin to destroy by ubiquitylation and then via proteosome.
When to divide
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It is necessary to divide cell within cell cycle. It begins at G1 stage. The cell is entered in
cell division as there is chromosomes in it. There are certain factors as well which state cell start
or not. In addition, single cell organism begins as well in it. As cell is surrounded by nutrients so
decide whether to divide or not (Salazar-Roa, and Malumbres, 2017). The molecules is divided
into 2 category that is mitogen and anti mitogen. These both allow in controlling cell division
and where cell divide.
How mitogen initiate cell division
They divide receptors which initiate signal transduction pathway. It leads to cyclin D-
Cdk4. This then results is activating cyclin E CDk2.
How mitogen increase cyclin D expression
There are few mitogens known as EGF which increase amount of cyclin D with help of
cyclin D gene. They initiate guanine nucleotide exchange factor for small GTP protein Ras.
Then, the ras GTP activate MAP kinase that results in activating cell transcription. Here, factors
in it are myc. It increases transcription of cyclin D. The ras, MAP myc are called as oncogenes.
How anti mitogens inhibit entry in cell cycle
The process initiate with when mitogen such as TGF and beta inhibit cell by restricting
cyclin D in Cdk4. The mitogen bind receptor that is called as Smad. But smad distance from
receptor and combine with smad4. It gets into nucleus to form protein known as lnk4. Then, lnk4
bind with cdk4 to which restrict to get combine from cyclin D. this is because cyclin D can not
combine with cdk4 and cyclin E does not enter cell (Venkei, and Yamashita, 2018).
How cyclin D Cdk4 activate cyclin E- cdk2
In order to generate cyclin E- cdk, cyclin D cdk surge transcription in cyclin E. however,
the cyclin E is controlled by factor that are E2F1 – 5. Furthermore, interaction of E2F with cyclin
E is regulated by protein that is retinoblastoma. When E2F 1 2 and 3 is bound by pRb it do not
connect with cyclin E but when E2F4 is bound then it bind cyclin E region. Therefore, pRb
presence cyclin E and cell are not able to divide. This is called as timor suppressor.
Positive feedback loop in cyclin E cdk2
It has been found that the loop also contributes in forming of cyclin E cdk2. It is found
that cyclin D cdk4 enable in making cyclin E and forming of cyclin D cdk2 as well. So, once cell
is activated then cyclin E cdk2 is able to maintain own activity. Here, mitogen is required to
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enhance cyclin D. hence, it is found that in most cell mitogen is not needed to move forward in
cell cycle.
Cell growth and cell division
Here, it is found that cell need macromolecule and organelles in order to enter into cell
cycle. So, mTor is kinase that combine with other protein. It results in forming of mTOR
complex. They play vital role in combing nutrition status of cell that increase protein and lipid.
The mTROC protein that is increase protein production. It activates factors of genes in lipid
synthesis. The mitogen turn signal to promote protein and lipid which support cell division.
Here, pathway is same that is used in insulin and insert GLUT4 in cell. Mitogen binds to a
tyrosine-kinase receptor, activating the receptor’s kinase domains and leading to cross-
phosphorylation of the cytosolic domains of the receptor. Here, phosphorylated protein obtain
protein in bind PI-3 kinase. Then, it converts PIP-2 into PIP-3. And initiate AKT. Hence,
mTORC rise production of protein as well as lipid (Overview of the Cell Cycle, 2019).
Cell cycle check point
Here, progress of cell is monitored by in next step. So, check point in this is DNA that
unattached chromosomes in mitosis. Thus, when it gets activate cell cycle is stopped to go in
next stage. Thus, by activating checkpoint cyclin CDK restrict to initiate cell to enter in next
cycle.
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REFERENCES
Books and journals
Cai, Y., and et.al., 2018. Experimental and computational framework for a dynamic protein atlas
of human cell division. Nature, 561(7723), pp.411-415.
Godard, B.G. and Heisenberg, C.P., 2019. Cell division and tissue mechanics. Current opinion in
cell biology, 60, pp.114-120.
Gudipaty, S.A., and et.al., 2017. Mechanical stretch triggers rapid epithelial cell division through
Piezo1. Nature, 543(7643), pp.118-121.
Salazar-Roa, M. and Malumbres, M., 2017. Fueling the cell division cycle. Trends in cell
biology, 27(1), pp.69-81.
Venkei, Z.G. and Yamashita, Y.M., 2018. Emerging mechanisms of asymmetric stem cell
division. Journal of Cell Biology, 217(11), pp.3785-3795.
Online
Overview of the Cell Cycle, 2019 [online] Available through :
<http://tbl.med.yale.edu/cell_growth_control/reading.php>
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