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Chapter 18 Cell Cycle-Control System and Interphase Phase
Terms in this set (29)
Cell Cycle Defined
refers to the series of coordinated events in which the cell duplicates its contents and divides in two.
For a cell to remain in equilibrium, it must double its mass each division cycle, including its organelles, proteins, and other biomolecules.
Cell Cycle Phases
-M Phase-nucleus and cell division; mitosis and cytokinesis
-Interphase-G1, G0, S, and G2 phase
the first cell divisions in animal embryos after fertilization in which the giant cell subdivides into smaller cells with little to no growth in the short G1 and G2 phases.
Regulatory steps that cells use in order to ensure that the cell cycle proceeds in the proper order.
Furthermore, the cell cycle control system monitors for damage, environmental signals, and for successful completion of one event before allowing the cycle to proceed to the next.
Three: G1, G2 and Mitosis Checkpoints
aka "Start". Cell confirms that nutrients and specific signal molecules in the extracellular environment are present to determine if conditions are favorable to commit to S phase. If not, may enter G0 phase.
Cell cycle control system ensures that all damaged DNA is repaired and all DNA is replicated before entering to the M phase of the cell cycle.
All replicated chromosomes must be properly attached to the mitotic spindle, before the spindle pulls the chromosomes apart into two daughter cells.
Major Cell Cycle Regulators
Cyclins and Cyclin-dependent protein kinases are the major regulators of cell cycle progressions.
cell-cycle regulatory proteins whose concentration gradually rises and falls at specific times in the cell cycle.
It binds to and activates specific cyclin-dependent protein kinases (Cdks).
Cyclin-dependent protein kinases (Cdks)
master regulators of the cell cycle that phosphorylate and regulate other proteins that act in the cell cycle. .
Cyclin-cdk complex consisting of M cyclin and cdk1 that act in G2 to trigger entry into M-phase
a protein phosphatase which removes an inhibitory protein on M-Cdk in order to activate it and trigger M-phase.
Possesses a positive feedback loop because active M-Cdk can phosphorylate inactive Cdc25 phosphatase, to activate it.
S-Cdk complex consists of S cyclins and Cdk2 that act in late G1 (along with G1/S-Cdk) to trigger S phase.
G1/S-Cdk complex consists of G1/S cyclins and Cdk2 that act in late G1 (along with S-Cdk) to trigger S phase.
G1-Cdk complex consists of G1 cyclins and Cdk4 and Cdk6 that acts in early G1 to drive cell through G1 towards S phase.
Formation usually depends on extracellular signal molecules that stimulate cells to divide (GFs).
In addition to cyclin binding, Cdks can also be activated or inhibited by phosphorylation, through the activity of protein phosphatases and other protein kinases.
Both activation and inactivation of Cdks are necessary for normal cell cycle progression each at a different site on the protein.
The abrupt drop in cyclin levels occurs through the ubiquitination of cyclins by enzymes that direct them to the proteasome for proteolysis.
This ensures that the cell cycle is irreversible and proceeds only in one direction.
Mammalian cells will only multiply if stimulated to do so by extracellular signals called mitogens. Without mitogens, the cell will arrest G1 checkpoint, and possibly enter the non-proliferating state G0 for some time.
Cdk Inhibitor proteins
are molecular brakes because they block the assembly or activity of one or more cyclin-Cdk complexes. This gives the cell more time to do complete certain tasks, like repair, grow or wait until extracellular conditions are favorable.
Neuronal and muscular cells stop dividing because many Cdks and cyclins disappear or are inhibited.
cell cycle phase in which DNA is replicated in preparation for cell division.
A key point is that chromosomes must be accurately replicated once and only once in each cell cycle or else this can have damaging gene amplification effects.
Origin Recognition Complex (ORC)
A multiprotein complex that remains bound to origins of replication sites through the cell cycle. Just prior to S phase, the ORC recruits other proteins necessary for initiation of replication to form the pre-replicative complex.
Pre-replicative complex (PRC)
is composed of the ORC with additional proteins necessary for initiation of replication prior to S phase.
The fully assembled PRC, can quickly respond to active S-Cdk to trigger S-Phase.
a key protein in the PRC, because it promotes binding of additional proteins necessary to form the PRC.
It also becomes phosphorylated shortly after S-Phase by S-Cdk, causing PRC to disassemble and marking Cdc6 for degradation-effectively ensuring replication is done only once per S-phase
During S phase, cohesin proteins form rings around the length of each sister chromatid pair. Holding them together until they separate in late mitosis.
DNA can be damaged by X-rays, UV, chemicals and more.
In order to prevent the passing on of mutations, DNA damage checkpoints act before and during S phase to shut of cell cycle and prevent replication of damaged DNA.
DNA damage can activate p53 to stop G1, or block Cdc25.
tumor suppressor protein, is important component of DNA damage checkpoints.
In response to DNA damage, p53 increases in concentration and activity by phosphorylation from protein kinases, p53 activates transcription of p21 Cdk inhibitor to arrest in G1, or if extensive damage is present induce apoptosis.
p21 protein becomes actively transcribed by p53.
p21 protein binds and inhibits active G1/S-Cdk and S-Cdk, which arrests the cell in G1 and allows time for damaged DNA to be repaired.
Missing or mutated p53 doesn't restrain replication of damage DNA which leads to high rate of mutation. Mutations in p53 are found in about half of all human cancers.
Incomplete DNA Replication
incompletely replicated DNA triggers a checkpoint that act to block Cdc25 phosphatase, which is required to remove inhibitory phosphatase on M-cdk
This prevents M-Cdk from becoming activated and triggering M-phase.
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