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BIO 140: Chapter 12
Terms in this set (22)
gap 1 between end of mitosis and S phase
-general cell growth
(synthesis phase) chromosome replication
Why do gap phases exist?
before mitosis can take place, the parent cell must grow large enough to divide into two cells that will be normal in size and function. The two gap phases provide the time required to accomplish these tasks
when non-dividing cells are stuck in G1, researchers refer to this arrested state as G0 state. Cells in G0 have effectively exited the cell cycle and are sometimes referred to as post-mitotic. Nerve cells, muscle cells and many other types of cells enter G0 once they have matured
M-Phase Promoting Factor (MPF)
complex of a cyclin and cyclin-dependent kinase that, when activated, phosphorylates a number of specific proteins needed to initiate mitosis in eukaryotic cells
-the cyclin subunit regulates the formation of the MPF dimer; the kinase subunit catalyzes the phosphorylation of other proteins to start M phase
-the concentration of the protein kinase is more or less constant throughout the cell cycle
How is MPF turned on? Why doesn't the increasing concentration of MPF during interphase trigger the onset of M phase?
the activity of MPF's Cdk subunit is further regulated by two phosphorylation events.
The phosphorylation of one site in Cdk activates the kinase, but when the second site is phosphorylated, it is inactivated. both sites are phosphorylated after cyclin binds to the Cdk. this allows the concentration of the dimer to increase without prematurely entering M phase. Late in G2 phase, an enzyme removes the inhibitory phosphate. this dephosphorylation reaction, coupled with the addition of the activating phosphate, changes the Cdk's shape in a way that turns on its kinase activity Once MPF is active, it triggers a series of events. Although the exact mechanisms involved are still under investigation, the result is that chromosomes begin to condense and the spindle apparatus starts to form. In this way, MPF triggers the onset of M phase
MPF deactivation illustrates two key concepts about regulatory systems in cells:
1. Negative Feedback: occurs when a process is slowed or shut down by one of its products. Thermostats shut down furnaces when temps are high; phosphofructokinase is inhibited by ATP; MPF is turned off by an enzyme complex that is activated by events in mitosis
2. Destroying specific proteins is a common way to control cell processes. In this case, the enzyme complex that is activated in anaphase attaches small proteins called ubiquitins to MPF's cyclin subunit. This marks the subunit for destruction by a protein complex called the proteasome
mass of cells formed by uncontrolled cell division. Can be benign or malignant
first checkpoint, occurring late in G1. for most cells this checkpoint is most important in establishing whether the cell will continue through the cycle and divide, or exit the cycle and enter G0.
Passes checkpoint if:
-cell size is adequate
-nutrients are sufficient
-social signals are present
-DNA is undamaged
A protein (e.g. p53) that prevents cell division, such as when the cell has DNA damage. Mutant genes that code for tumor suppressors are associated with cancer
second checkpoint occurs after S phase, at the boundary between the G2 and M phases.
-chromosomes have replicated successfully
-activated MPF is present
at metaphase and anaphase
-chromosomes have attached to spindle apparatus
-chromosomes have properly segregated and MPF is absent
If metaphase checkpoint didn't exist, some chromosomes might not separate correctly, and daughter cells would receive either too many too few chromosomes
If chromosomes do not fully separate during anaphase, MPF will not decline and the cell will be arrested in M phase.
general term for disease caused by cells that divide in an uncontrolled fashion, invade nearby tissues, and spread to other sites in the body
-many types of cancer involve defects in G1 checkpoint
Cancerous cells have two types of defects related to cell division:
1. defects that make the proteins required for cell growth active when they shouldn't be
2. defects that prevent tumor suppressor genes from shutting down the cell cycle
any of a large number of signaling molecules that are secreted by certain cells and that stimulate other cells to grow, divide, or differentiate
How do social controls and cell cycle checkpoints fail?
-cells can become cancerous when social controls fail--meaning, when cells begin to divide in the absence of the go-ahead signal from growth factors
-One of two things can go wrong: the G1 cyclin is overproduced, or RB is defective
Cyclin overproduction results from
1. excessive amounts of growth factors, or
2. cyclin production in the absence of growth signals. Cyclins are produced continuously when a signaling pathway is defective. Because this pathway includes the Ras protein, it is common to find overactive Ras proteins in cancerous cells
What happens when Rb is defective?
when Rb is missing or does not bind normally to E2F, any E2F that is present pushes the cell through the G1 checkpoint and into S phase, leading to uncontrolled cell division
For the cell, why is it better to be held in the G1 phase than S, G2 or M phase?
G1 cells have not replicated their DNA in preparation for division.
Which type of molecule catalyzes the phosphorylation of other proteins to start M phase?
How would the removal of growth factors affect asynchronous cultures of (1) normal human cells and (2) most human cancer cells?
(1) Arrest in G1; (2) no effect
What would happen if the kinase that adds the inhibitory phosphate to Cdk were defective?
M phase would begin prematurely.