chapter 12. cell division – why? growth repair reproduction
TRANSCRIPT
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Chapter 12
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Cell Division – Why?GrowthRepairReproduction
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The Cell CycleFrequency of division varies by cell type
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InterphaseLongest phase (90% of cell cycle)DNA is loosely packed (chromatin)Nucleus is well-definedThree parts:
G1 (Gap 1)S (Synthesis)G2 (Gap 2)
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M PhaseTwo parts:
Mitosis (division of nucleus)Cytokinesis (division of cytoplasm)
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ProphaseCondensation of DNA
HistonesNucleosomesChromatinChromosomes
Sister chromatids Centromere Kinetochores
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PrometaphaseNucleus breaks downCentrioles move to polesSpindle fibers form and attach to kinetochore
proteins
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MetaphaseMetaphase plate
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AnaphaseInactivation of proteins
holding chromatids together
Chromatids pulled by motor proteins to opposite poles
Polar spindle fibers elongate
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TelophaseFormation of daughter nucleiSpindle fibers disintegrateDNA uncoilsCytokinesis occurs simultaneously
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CytokinesisAnimals: Actin ring forms cleavage furrowPlants: Golgi sends vesicles forming cell
plate
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Evolution of MitosisBinary fission
(prokaryotes)Intact nuclear envelope
(some protists)Mitosis
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Cell Cycle ControlTwo irreversible points in
cell cycleReplication of genetic
materialSeparation of chromatids
Can be paused at checkpointsChemical signals indicate
cell processes are completed correctly
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3 Critical CheckpointsG1 (AKA “restriction point”) most critical
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“Go-ahead Signals”Usually proteins or steroid hormonesIntracellular signals: “promoting factors”External signals: “growth factors”Primary mechanism of control:
phosphorylation by kinase enzymes
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Promoting FactorsCyclin – regulatory proteinCdk’s – cyclin-dependent
kinasesActivate cyclinCyclin + cdk = MPF (Mitosis
Promoting Factor)APC (Anaphase Promoting
Complex)
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Growth FactorsExtracellular signals that
stimulate other cells to divide
Density-dependent inhibition
Anchorage dependence
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Cancerp53 & G1 checkpoint
Apoptosis or repairBenign tumors Malignant tumors
(metastasis)
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Growth Factors & CancerProto-oncogenes
Promote cell divisionCancerous if mutated
“on”Example: RAS
(activates cyclins)Tumor suppressor
genesCancerous if mutated
“off”Example: p53
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Development of CancerDevelops only after a cell experiences ~6 key
mutationsUnlimited growth - turn on growth promoter genesIgnore checkpoints - turn off tumor suppressor genesEscape apoptosis - turn off suicide genesImmortality = unlimited divisions -turn on telomerasePromotes blood vessel growth - turn on blood vessel
growth genesOvercome anchor & density dependence - turn off
touch sensor gene
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Kidney Cells
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Liver Cells
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Blood Cells
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Colon Cells
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Questions to DiscussWhat are the general defining features of
normal cells?What are the general defining features of cancer
cells?How does the chromosomal composition differ
between normal and cancerous cells?How does the actual process of cell division
differ in cancerous cells from that of normal cells?
What other questions about cancer do you have?
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Questions to DiscussWas it right to take Henrietta Lacks’s cells
without permission? Why or why not?Should the family have been told sooner?Is the surviving family entitled to any
compensation? If so, what?Hundreds of medical and biological advances
have been made that wouldn’t have happened without HeLa cells. How does that affect your answer?
If the family decided that they didn’t want HeLa cells being used any more, do you think it is within their right to demand it? Why or why not?