Transcript Chapter 12. Regulation of the Cell Cycle

Cell Cycle Regulation
[Ch 9]
different cells divide at different rates
AP Biology
2007-2008
Control  2 checkpoints
1. G1/S  DNA replication
2. G2/M Checkpoint  separation of sister
chromatids

If DNA synthesis is correct, mitosis starts
sister chromatids
centromere
single-stranded
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chromosomes

double-stranded
chromosomes

G1/S checkpoint
 most critical checkpoint
Go signal = it divides
 No signal = exits cycle & switches to G0

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G0 phase
 non-dividing state
 most human cells in G0 phase
M
Mitosis
G2
Gap 2
S
Synthesis
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 nerve & muscle cells
 in G0 & never divide
G1
Gap 1
G0
Resting
Cell Communication
how cells know when to divide
 Cells communicate with signals
 Signals are proteins that can be . . .
activators [go]
 inhibitors [stop]

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“Go” signals
 internal signals = “promoting” factors
 external signals = “growth” factors
 How do signals work?

phosphorylation
 kinase enzymes
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inactivated Cdk
Signal Types
 cyclin
regulatory protein
 bind to kinase enzyme

 Cdk

cyclin-dependent kinase

Enzyme  cascade
activated Cdk
 Cdk-cyclin complex

triggers passage through different
stages of cell cycle
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
regulation of cell cycle is
so key to life that the
genes for these
regulatory proteins have
been highly conserved
through evolution

the genes are basically
the same in yeast,
insects, plants & animals
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Growth factor signals  cells tell other cells when to divide
growth factor
nuclear pore
nuclear membrane
P
P
cell division
cell surface
receptor
protein kinase
cascade
Cdk
P
P
E2F
chromosome
P
APcytoplasm
Biology
nucleus
Example
 Platelet Derived Growth Factor (PDGF)

binding of PDGF to receptors stimulates cell
division in connective tissue
 heal wounds
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Cancer
 proto-oncogenes
growth factor genes become oncogenes
(cancer-causing) when mutated
 if switched “ON”  stimulates cell growth

 tumor-suppressor genes
genes inhibit cell division
 if switched “OFF” can cause cancer  cell
division is not inhibited like it should be

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Cancer & Cell Growth
 Cancer = failure to CONTROL
cell division
 How?


lose checkpoints
gene p53 plays a key role in G1/S restriction point
 p53 protein halts cell division if it detects damaged DNA




stimulates repair enzymes to fix DNA
forces cell into G0 resting stage
keeps cell in G1 arrest
causes apoptosis of damaged cell
 ALL cancers have to shut down p53 activity
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p53 — master regulator gene
NORMAL p53
p53 allows cells
with repaired
DNA to divide.
p53
protein
DNA repair enzyme
p53
protein
Step 1
Step 2
Step 3
DNA damage is caused
by heat, radiation, or
chemicals.
Cell division stops, and
p53 triggers enzymes to
repair damaged region.
p53 triggers the destruction
of cells damaged beyond repair.
ABNORMAL p53
abnormal
p53 protein
Step 1
DNA damage is
caused by heat,
radiation, or
AP chemicals.
Biology
cancer
cell
Step 2
The p53 protein fails to stop
cell division and repair DNA.
Cell divides without repair to
damaged DNA.
Step 3
Damaged cells continue to divide.
If other damage accumulates, the
cell can turn cancerous.