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• Who has a bigger cell? Elephant or Mouse?
• Why do cells divide instead of just growing bigger?– The larger the cell, the more demands it
places on DNA• Small cells, the DNA can meet the needs of the cell• As cell grows, the DNA can not meet the needs of
the cell – does not make extra copies of DNA to meet needs
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Cell Size
• The larger the cell, the more difficult it is to transport nutrients and waste across the cell membrane. The cell membrane’s inefficiency increases– Exchange rate of materials is dependent on
the surface area• S.A. = Length X Width X # of sides
– The rate of materials used and waste produced is dependent on volume
• Volume = Length X Width X Height
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• Understanding the relationship between surface area to volume is the key to understanding why cells must divide as they grow
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The Cell CycleThe Cell Cycle (Movie)
• Normal growth, development, and maintenance depend on the timing and rate of mitosis (cell division). Various cells differ in their pattern of cell division:
• Human skin cells → frequent• Liver cells → only in appropriate situations• Nerve cells → do not divide in mature
humans
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AP Biology
G2
S G1
Mmetaphase
prophase
anaphasetelophas
e
interphase (G1, S, G2 phases)mitosis (M)cytokinesis (C)
C
▪ Frequency of cell division varies by cell type◆ embryo
▪ cell cycle < 20 minute◆ skin cells
▪ divide frequently throughout life▪ 12-24 hours cycle
◆ liver cells▪ retain ability to divide, but keep it in reserve▪ divide once every year or two
◆ mature nerve cells & muscle cells▪ do not divide at all after maturity▪ permanently in G0
Frequency of cell division
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Fig. 12-5
S(DNA synthesis)
MITOTIC(M) PHASE
Mitosi
sCytokinesis
G1
G2
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Checkpoints
• The cell cycle is regulated by a molecular signaling system which switches the cell cycle control system on/off.
• The system consists of a molecular clock and checkpoints to ensure conditions are met before moving on to the next steps.
• Malfunctions may lead to cancer.
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AP Biology
Overview of Cell Cycle Control▪ Two irreversible points in cell cycle◆ replication of genetic material◆ separation of sister chromatids▪ Checkpoints ◆ process is assessed & possibly halted
centromere
sister chromatids
single-strandedchromosomes double-stranded
chromosomes
There’s noturning back,now!
✓ ✓
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Fig. 12-14
SG1
M checkpoint
G2M
Controlsystem
G1 checkpoint
G2 checkpoint
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Cycle Phases
• G1 – First growth phase. Metabolic activity proceeds at a normal rate. Duration highly variable. Synthesis of enzymes related to DNA replication.
• G0 – Quiescent (rest) state. Usually for non-proliferative cells. Can occur for cells that are damaged. Alternative to apoptosis. Can be temporary or permanent.
• Nerve and muscle cells (multinucleated)
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• S – DNA replication. – All chromosomes replicated. – Chromosomes consist of 2 sister chromatids in
chromatin form. – Histones produced.Chromosome
• 1 long string of DNA Sister chromatids
• Loose- chromatin• Tight - chromatid
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Fig. 12-4 0.5 µm Chromosomes
Chromosomeduplication(including DNAsynthesis)
Chromo-some arm
Centromere
Sisterchromatids
DNA molecules
Separation ofsister chromatids
Centromere
Sister chromatids
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• G2 – Second growth phase. – Reproduction of some organelles. High microtubule
production. – Two centrosomes. Aster around each centrosome.
Cells grow in size.• M – Mitosis.
– Prophase, Prometaphase, Metaphase, Anaphase, Telophase
• Cytokinesis– Birth of 2 daughter cells
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Fig. 12-7
Microtubules Chromosomes
Sisterchromatids
Aster
Metaphaseplate
Centrosome
Kineto-chores
Kinetochoremicrotubules
Overlappingnonkinetochoremicrotubules
Centrosome 1 µm
0.5 µm
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Internal and External Signals for Mitosis
• Growth Factors• Density-dependent inhibition
– Crowded cells stop dividing• Anchorage dependence
– Must be attached to … • ECM or culture of a jar
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The Cell Cycle Clock/Checkpoints2 Types of Regulatory Molecules, together act as a
checkpoint1) Kinases– Amount doesn’t fluctuate– enzymes that phosphorylates molecules– Cyclin dependent kinase (Cdk) – inactive (G1 & G2) until cyclin
are present 2) Cyclins
– Molecule concentration fluctuates (unlike kinase)– Bonds w/ Kinase and serves a checkpoint– Cyclin-Cdk complex (MPF M-phase promoting factor) promotes
certain activities that eventually lead to the next stage of the cell cycle
– Having the minimum concentration of these complexes help the cell cycle proceed through the checkpoints
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Actual Checkpoints
• Click on normal cell division (top left)
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Steps of the Cell Cycle
• Sometime after cytokinesis G1 cyclins rise and bind to their Cdks (activates Cdks) which signals the cell to prepare for chromosome replication.– This moves cell past G1 checkpoint
• “S” phase promoting factor (SPF) enters the nucleus, prepares the cell to duplicate its DNA and centrosomes – S phase begins -
• S-cyclin-Cdk complexes form. They phosphorylate proteins that ensure DNA replication.
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Fig. 12-17M G1 S G2 M G1 S G2 M G1
MPF activity
Cyclinconcentration
Time(a) Fluctuation of MPF activity and cyclin concentration
during the cell cycle
Degradedcyclin
Cdk
G 1S
G 2
M
CdkG2checkpointCyclin is
degraded
CyclinMPF
(b) Molecular mechanisms that help regulate the cell cycle
Cyclin accum
ulation
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In depth Animation• During G2, M-phase cyclins begin to rise and form
Mitosis promoting factors (MPF) (M cyclin Cdk complexes).
• G2 checkpoint: Checks for DNA damage. • Then MPF initiates assembly of mitotic spindle, the
breakdown of the nuclear envelope, cessation of gene transcription, and condensation of the chromosomes, and taking the cell cycle all the way to metaphase.
• M checkpoint: All chromosomes are aligned at the metaphase plate,
• MPF activates the Anaphase Promoting Complex (APC) which allows sister chromatids to separate which activates G1 cyclins, and degrades M cyclins.
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Quality Control• Systems for interrupting the cell cycle if
something goes wrong1) DNA damage checkpoint
1) happens at G1 checkpoint + S phase + M phase2) P53 gene – tumor suppresor
2) Completion of S-phase1) Makes sure that there are no okazaki fragments
3) Spindle Checkpoint1) Assures spindles are properly connected to
kinetichore• If problem cannot be fixed, the cell signals for
apoptosisIf problem cannot be fixed, the cell signals for apoptosis - Movie
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Cancer• A group of diseases that involve irregular growth
and reproduction of cells• Cancer occurs when genes involved in the cycle,
specifically with check points are altered (growth factors)
• Transformation – single cell converts to a cancer cell
• Benign Tumor – a group of abnormal cells that does not invade other body systems- not considered cancerous
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• Metastasis – when cancerous cells break off the original tumor and travel to other parts of the body
• Malignant Tumor – a tumor that invades a body system by traveling via the bloodstream or the lymphatic system
• Cancer causes death b/c the cells take over the function of organs
• Cancer arises due to damage to genes (90%) or inheritance (10)
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Fig. 12-20
Tumor
A tumor growsfrom a singlecancer cell.
Glandulartissue
Lymphvessel
Bloodvessel
Metastatictumor
Cancercell
Cancer cellsinvade neigh-boring tissue.
Cancer cells spreadto other parts ofthe body.
Cancer cells maysurvive andestablish a newtumor in anotherpart of the body.
1 2 3 4
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AP Biology
Growth Factors and Cancer▪ Growth factors can create cancers◆ proto-oncogenes
▪ normally activates cell division • growth factor genes • become Oncogenes (cancer-causing) when mutated
▪ if switched “ON” can cause cancer▪ example: RAS (activates cyclins)
◆ Tumor Suppressor Genes ▪ normally inhibits cell division▪ if switched “OFF” can cause cancer. Why?▪ example: p53
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AP Biology
Cancer & Cell Growth▪ Cancer is essentially a failure
of cell division control ◆ unrestrained, uncontrolled cell growth
▪ What control is lost?◆ lose checkpoint stops◆ gene p53 plays a key role in G1/S restriction point
▪ p53 protein halts cell division if it detects damaged DNA • options:
■ 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▪ Inhibits blood vessel growth in tumors (angiogenesis)
p53 discovered at Stony Brook by Dr. Arnold Levine
p53 is theCell CycleEnforcer
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AP Biology
DNA damage is causedby heat, radiation, or chemicals.
p53 allows cellswith repairedDNA to divide.
Step 1
DNA damage iscaused by heat,radiation, or chemicals.
Step 1
Step 2
Damaged cells continue to divide.If other damage accumulates, thecell can turn cancerous.
Step 3p53 triggers the destruction
of cells damaged beyond repair.
ABNORMAL p53
NORMAL p53
abnormalp53 protein
cancercell
Step 3
The p53 protein fails to stopcell division and repair DNA.Cell divides without repair todamaged DNA.
Cell division stops, and p53 triggers enzymes to repair damaged region.
Step 2
DNA repair enzymep53protein p53
protein
p53 — master regulator gene
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AP Biology
Development of Cancer▪ Cancer develops only after a cell experiences
~6 key mutations (“hits”)◆ unlimited growth
▪ turn on growth promoter genes◆ ignore checkpoints
▪ turn off tumor suppressor genes (p53)◆ escape apoptosis
▪ turn off suicide genes◆ immortality = unlimited divisions
▪ turn on chromosome maintenance genes◆ promotes blood vessel growth
▪ turn on blood vessel growth genes◆ overcome anchor & density dependence
▪ turn off touch-sensor gene
It’s like anout-of-contro
lcar with many
systems failing!
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AP Biology
What causes these “hits”? ▪ Mutations in cells can be triggered by
◆ UV radiation◆ chemical exposure◆ radiation exposure◆ heat
◆ cigarette smoke◆ pollution◆ age◆ genetics
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AP Biology
Tumors▪ Mass of abnormal cells◆ Benign tumor
▪ abnormal cells remain at original site as a lump
• p53 has halted cell divisions▪ most do not cause serious problems &
can be removed by surgery◆ Malignant tumor
▪ cells leave original site• lose attachment to nearby cells • carried by blood & lymph system to other tissues• start more tumors = metastasis
▪ impair functions of organs throughout body
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Mitosis
• Mitosis – reproduction of the nucleus• Cytokinesis – division of the cytoplasm• Diploid (2n) – cells that have 2 sets of
chromosomes (46)• Haploid (n) - cells that have 1 set of
chromosomes (23)• Somatic cells – cells that only undergo
mitosis
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Diploid – 2n
• M1 + D1 are homologous• Zygote = egg + sperm
• Allele: different versions of the same trait
m1 m2 m3 D1 D2 D3
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• During G2 -Tetraploid – 4n
46 – double stranded chromosomes
m1 m1 D1 D1
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• Egg and Sperm produced in Meiosis (haploid)
+Egg (n) Sperm (n)
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Stage
• G1 – Diploid (2n)• S – Tetraploid (4n) Interphase• G2 – Tetraploid• Mitosis…
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Prophase-
-Chromatin fibers begin to condense into chromosomes and wind around histone proteins.
-Nucleoli disappears.
-Chromosomes become visible. Chromatid arms held together by cohesions (vertebrates only at the centromere).
-Mitotic spindle forms, extending from the centrosomes outside the nucleus forming asters. Centrioles (found in animal and lower plant cells) are in the center of the centrosome.
-The centrosomes are moving to opposite poles.
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Prometaphase
-The nuclear envelopes fragments and nucleolus is not longer visible.
-Centrosomes are at opposite ends of the nuclear area.
-The microtubules extend through the nuclear area
-2 Kinetochores (facing opposite from one another) form on the centromere. These are protein structures that allow microtubules to attach.
-Kinetochore microtubules attach to the kinetochores. Moving the chromosomes back and forth until they reach the middle of the cell.
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Metaphase-
-Longest phase of mitosis.
-The “tug and pull” of the kinetochore microtubules brings the twin chromatids to the metaphase plate.
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Anaphase-
-Cohesion proteins are cleaved and the sister chromatids separate. The chromatids become chromosomes in their own right.
-The chromosomes begin to move to opposite poles. The chromosomes are “walking” up the kinetochore microtubules.
-The kinetochore microtubules are disassembled at the chromosome end.
-The nonkinetochore microtubules move further apart as the interact with one another. More subunits are attached to the overlapping end. This causes the cell to enlarge.
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This experiment shows that the microtubules are disassembled at the chromosome end and not the centrosome end. The spindle fiber were marked in the middle. If the microtubules shorten between the mark and centrosome, then the microtubules are being reeled in but if the microtubules shorten between the mark and the chromosomes, then microtubules are being disassembled at that end. The latter is the case. The kinetochore disassembles the microtubules at the chromosome end, as the chromosome “walks” up the microtubule.
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Telophase
-Two daughter nuclei form in the cell.
-Nuclear envelope forms from the fragments of the disassembled nuclei and the endomembrane system.
-Chromosomes unwind forming chromatin.
-Beginning of cytokinesis
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Mitosis without cytokinesis results in coencytic bodies without individual cells.
Happens in some plants, fungi, algae and even a few animals. Animals cells do cytokinesis by the pinching in of the cell membrane.
In animal cells, rings of actin form under the cell membrane associated with myosin (much like skeletal muscles) contracts like a “pull-string” purse. This forms a cleavage furrow.
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Cell Plate in plant cells forms by fusing vesicles produced by the golgi
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Fig. 12-9
Cleavage furrow100 μm
Contractile ring ofmicrofilaments
Daughter cells
(a) Cleavage of an animal cell (SEM) (b) Cell plate formation in a plant cell (TEM)
Vesiclesformingcell plate
Wall ofparent cell
Cell plate
Daughter cells
New cell wall
1 μm
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