chapter 12. cell division – why? growth repair reproduction

Chapter 12

Cell Division – Why?GrowthRepairReproduction

The Cell CycleFrequency of division varies by cell type

InterphaseLongest phase (90% of cell cycle)DNA is loosely packed (chromatin)Nucleus is well-definedThree parts:

G1 (Gap 1)S (Synthesis)G2 (Gap 2)

M PhaseTwo parts:

Mitosis (division of nucleus)Cytokinesis (division of cytoplasm)

ProphaseCondensation of DNA

HistonesNucleosomesChromatinChromosomes

Sister chromatids Centromere Kinetochores

PrometaphaseNucleus breaks downCentrioles move to polesSpindle fibers form and attach to kinetochore

proteins

MetaphaseMetaphase plate

AnaphaseInactivation of proteins

holding chromatids together

Chromatids pulled by motor proteins to opposite poles

Polar spindle fibers elongate

TelophaseFormation of daughter nucleiSpindle fibers disintegrateDNA uncoilsCytokinesis occurs simultaneously

CytokinesisAnimals: Actin ring forms cleavage furrowPlants: Golgi sends vesicles forming cell

plate

Evolution of MitosisBinary fission

(prokaryotes)Intact nuclear envelope

(some protists)Mitosis

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

3 Critical CheckpointsG1 (AKA “restriction point”) most critical

“Go-ahead Signals”Usually proteins or steroid hormonesIntracellular signals: “promoting factors”External signals: “growth factors”Primary mechanism of control:

phosphorylation by kinase enzymes

Promoting FactorsCyclin – regulatory proteinCdk’s – cyclin-dependent

kinasesActivate cyclinCyclin + cdk = MPF (Mitosis

Promoting Factor)APC (Anaphase Promoting

Complex)

Growth FactorsExtracellular signals that

stimulate other cells to divide

Density-dependent inhibition

Anchorage dependence

Cancerp53 & G1 checkpoint

Apoptosis or repairBenign tumors Malignant tumors

(metastasis)

Growth Factors & CancerProto-oncogenes

Promote cell divisionCancerous if mutated

“on”Example: RAS

(activates cyclins)Tumor suppressor

genesCancerous if mutated

“off”Example: p53

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

Kidney Cells

Liver Cells

Blood Cells

Colon Cells

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?

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?