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Mechanisms of cell cycle control

As the cell proceeds through its cycle, each phase involves certain processes that must be completed before the cell should advance to the next phase. A checkpoint    is a point in the cell cycle at which the cycle can be signaled to move forward or stopped. At each of these checkpoints, different varieties of molecules provide the stop or go signals, depending on certain conditions within the cell. A cyclin    is one of the primary classes of cell cycle control molecules ( [link] ). A cyclin-dependent kinase (CDK)    is one of a group of molecules that work together with cyclins to determine progression past cell checkpoints. By interacting with many additional molecules, these triggers push the cell cycle forward unless prevented from doing so by “stop” signals, if for some reason the cell is not ready. At the G 1 checkpoint, the cell must be ready for DNA synthesis to occur. At the G 2 checkpoint the cell must be fully prepared for mitosis. Even during mitosis, a crucial stop and go checkpoint in metaphase ensures that the cell is fully prepared to complete cell division. The metaphase checkpoint ensures that all sister chromatids are properly attached to their respective microtubules and lined up at the metaphase plate before the signal is given to separate them during anaphase.

Control of the cell cycle

This image shows the different stages of the cell cycle along with the checkpoints between them and the cyclins responsible for the checkpoint at each stage.
Cells proceed through the cell cycle under the control of a variety of molecules, such as cyclins and cyclin-dependent kinases. These control molecules determine whether or not the cell is prepared to move into the following stage.

The cell cycle out of control: implications

Most people understand that cancer or tumors are caused by abnormal cells that multiply continuously. If the abnormal cells continue to divide unstopped, they can damage the tissues around them, spread to other parts of the body, and eventually result in death. In healthy cells, the tight regulation mechanisms of the cell cycle prevent this from happening, while failures of cell cycle control can cause unwanted and excessive cell division. Failures of control may be caused by inherited genetic abnormalities that compromise the function of certain “stop” and “go” signals. Environmental insult that damages DNA can also cause dysfunction in those signals. Often, a combination of both genetic predisposition and environmental factors lead to cancer.

The process of a cell escaping its normal control system and becoming cancerous may actually happen throughout the body quite frequently. Fortunately, certain cells of the immune system are capable of recognizing cells that have become cancerous and destroying them. However, in certain cases the cancerous cells remain undetected and continue to proliferate. If the resulting tumor does not pose a threat to surrounding tissues, it is said to be benign and can usually be easily removed. If capable of damage, the tumor is considered malignant and the patient is diagnosed with cancer.

Homeostatic imbalances

Cancer arises from homeostatic imbalances

Cancer is an extremely complex condition, capable of arising from a wide variety of genetic and environmental causes. Typically, mutations or aberrations in a cell’s DNA that compromise normal cell cycle control systems lead to cancerous tumors. Cell cycle control is an example of a homeostatic mechanism that maintains proper cell function and health. While progressing through the phases of the cell cycle, a large variety of intracellular molecules provide stop and go signals to regulate movement forward to the next phase. These signals are maintained in an intricate balance so that the cell only proceeds to the next phase when it is ready. This homeostatic control of the cell cycle can be thought of like a car’s cruise control. Cruise control will continually apply just the right amount of acceleration to maintain a desired speed, unless the driver hits the brakes, in which case the car will slow down. Similarly, the cell includes molecular messengers, such as cyclins, that push the cell forward in its cycle.

In addition to cyclins, a class of proteins that are encoded by genes called proto-oncogenes provide important signals that regulate the cell cycle and move it forward. Examples of proto-oncogene products include cell-surface receptors for growth factors, or cell-signaling molecules, two classes of molecules that can promote DNA replication and cell division. In contrast, a second class of genes known as tumor suppressor genes sends stop signals during a cell cycle. For example, certain protein products of tumor suppressor genes signal potential problems with the DNA and thus stop the cell from dividing, while other proteins signal the cell to die if it is damaged beyond repair. Some tumor suppressor proteins also signal a sufficient surrounding cellular density, which indicates that the cell need not presently divide. The latter function is uniquely important in preventing tumor growth: normal cells exhibit a phenomenon called “contact inhibition;” thus, extensive cellular contact with neighboring cells causes a signal that stops further cell division.

These two contrasting classes of genes, proto-oncogenes and tumor suppressor genes, are like the accelerator and brake pedal of the cell’s own “cruise control system,” respectively. Under normal conditions, these stop and go signals are maintained in a homeostatic balance. Generally speaking, there are two ways that the cell’s cruise control can lose control: a malfunctioning (overactive) accelerator, or a malfunctioning (underactive) brake. When compromised through a mutation, or otherwise altered, proto-oncogenes can be converted to oncogenes, which produce oncoproteins that push a cell forward in its cycle and stimulate cell division even when it is undesirable to do so. For example, a cell that should be programmed to self-destruct (a process called apoptosis) due to extensive DNA damage might instead be triggered to proliferate by an oncoprotein. On the other hand, a dysfunctional tumor suppressor gene may fail to provide the cell with a necessary stop signal, also resulting in unwanted cell division and proliferation.

A delicate homeostatic balance between the many proto-oncogenes and tumor suppressor genes delicately controls the cell cycle and ensures that only healthy cells replicate. Therefore, a disruption of this homeostatic balance can cause aberrant cell division and cancerous growths.

Visit this link to learn about mitosis. Mitosis results in two identical diploid cells. What structures forms during prophase?

Chapter review

The life of cell consists of stages that make up the cell cycle. After a cell is born, it passes through an interphase before it is ready to replicate itself and produce daughter cells. This interphase includes two gap phases (G 1 and G 2 ), as well as an S phase, during which its DNA is replicated in preparation for cell division. The cell cycle is under precise regulation by chemical messengers both inside and outside the cell that provide “stop” and “go” signals for movement from one phase to the next. Failures of these signals can result in cells that continue to divide uncontrollably, which can lead to cancer.

Once a cell has completed interphase and is ready for cell division, it proceeds through four separate stages of mitosis (prophase, metaphase, anaphase, and telophase). Telophase is followed by the division of the cytoplasm (cytokinesis), which generates two daughter cells. This process takes place in all normally dividing cells of the body except for the germ cells that produce eggs and sperm.

Visit this link to learn about mitosis. Mitosis results in two identical diploid cells. What structures form during prophase?

the spindle

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Questions & Answers

Three charges q_{1}=+3\mu C, q_{2}=+6\mu C and q_{3}=+8\mu C are located at (2,0)m (0,0)m and (0,3) coordinates respectively. Find the magnitude and direction acted upon q_{2} by the two other charges.Draw the correct graphical illustration of the problem above showing the direction of all forces.
Kate Reply
To solve this problem, we need to first find the net force acting on charge q_{2}. The magnitude of the force exerted by q_{1} on q_{2} is given by F=\frac{kq_{1}q_{2}}{r^{2}} where k is the Coulomb constant, q_{1} and q_{2} are the charges of the particles, and r is the distance between them.
Muhammed
What is the direction and net electric force on q_{1}= 5µC located at (0,4)r due to charges q_{2}=7mu located at (0,0)m and q_{3}=3\mu C located at (4,0)m?
Kate Reply
what is the change in momentum of a body?
Eunice Reply
what is a capacitor?
Raymond Reply
Capacitor is a separation of opposite charges using an insulator of very small dimension between them. Capacitor is used for allowing an AC (alternating current) to pass while a DC (direct current) is blocked.
Gautam
A motor travelling at 72km/m on sighting a stop sign applying the breaks such that under constant deaccelerate in the meters of 50 metres what is the magnitude of the accelerate
Maria Reply
please solve
Sharon
8m/s²
Aishat
What is Thermodynamics
Muordit
velocity can be 72 km/h in question. 72 km/h=20 m/s, v^2=2.a.x , 20^2=2.a.50, a=4 m/s^2.
Mehmet
A boat travels due east at a speed of 40meter per seconds across a river flowing due south at 30meter per seconds. what is the resultant speed of the boat
Saheed Reply
50 m/s due south east
Someone
which has a higher temperature, 1cup of boiling water or 1teapot of boiling water which can transfer more heat 1cup of boiling water or 1 teapot of boiling water explain your . answer
Ramon Reply
I believe temperature being an intensive property does not change for any amount of boiling water whereas heat being an extensive property changes with amount/size of the system.
Someone
Scratch that
Someone
temperature for any amount of water to boil at ntp is 100⁰C (it is a state function and and intensive property) and it depends both will give same amount of heat because the surface available for heat transfer is greater in case of the kettle as well as the heat stored in it but if you talk.....
Someone
about the amount of heat stored in the system then in that case since the mass of water in the kettle is greater so more energy is required to raise the temperature b/c more molecules of water are present in the kettle
Someone
definitely of physics
Haryormhidey Reply
how many start and codon
Esrael Reply
what is field
Felix Reply
physics, biology and chemistry this is my Field
ALIYU
field is a region of space under the influence of some physical properties
Collete
what is ogarnic chemistry
WISDOM Reply
determine the slope giving that 3y+ 2x-14=0
WISDOM
Another formula for Acceleration
Belty Reply
a=v/t. a=f/m a
IHUMA
innocent
Adah
pratica A on solution of hydro chloric acid,B is a solution containing 0.5000 mole ofsodium chlorid per dm³,put A in the burret and titrate 20.00 or 25.00cm³ portion of B using melting orange as the indicator. record the deside of your burret tabulate the burret reading and calculate the average volume of acid used?
Nassze Reply
how do lnternal energy measures
Esrael
Two bodies attract each other electrically. Do they both have to be charged? Answer the same question if the bodies repel one another.
JALLAH Reply
No. According to Isac Newtons law. this two bodies maybe you and the wall beside you. Attracting depends on the mass och each body and distance between them.
Dlovan
Are you really asking if two bodies have to be charged to be influenced by Coulombs Law?
Robert
like charges repel while unlike charges atttact
Raymond
What is specific heat capacity
Destiny Reply
Specific heat capacity is a measure of the amount of energy required to raise the temperature of a substance by one degree Celsius (or Kelvin). It is measured in Joules per kilogram per degree Celsius (J/kg°C).
AI-Robot
specific heat capacity is the amount of energy needed to raise the temperature of a substance by one degree Celsius or kelvin
ROKEEB
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Source:  OpenStax, Anatomy & Physiology. OpenStax CNX. Feb 04, 2016 Download for free at http://legacy.cnx.org/content/col11496/1.8
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