Jill before teaching go to this
hyperlink (on these words)
THE CELL CYCLE
Chapter 9
Continuous balance between cell division and cell death
 Mitosis – A process that forms two genetically
identical cells from one
 Product of mitosis: daughter cells
 Apoptosis – natural cell death – precise –
geneticallly programmed(?)
The Cell Cycle (hyperlink)
Checkpoints – 1. when certain proteins interact
in a way that ensures the proper sequence
of events is unfolding
2. allows a pause so newly formed DNA can
be checked and repaired before dictating
orders
Cell cycle, con’t
Events that occur in the life of a cell.
Includes 3 major stages:
• Interphase
• Karyokinesis (mitosis)
• Cytokinesis
Interphase
•
Cell is not dividing, but there is GREAT activity
G1 Phase - carries out basic functions & performs
specialized activities.
• duration is extremely variable
• Synthesizes proteins, lipids and carb in case of
cell division
G1 Phase, con’t
contains restriction checkpoint ~ cell “decides” to:
- Divide
- Stops to repair DNA damage
- enter a quiescent phase (G0)
- die
Interphase, con’t
G0 Phase – a cell can exit the cycle at G1 to enter
this phase
• The cell maintains specialized characteristics,
but does not divide.
• No replication of DNA
• Must be at this stage in an egg for cloning to
work
Ex. neurons & muscle cells
Interphase, con’t
Phase –
•Great Synthetic activity – replicating
DNA
• cell replicates chromosomes &
synthesizes associated proteins. (also
those that coordinate events of nucleus
and cytoplasm
(animal cells replicate
centrioles as well)
•S
G2 Phase –
• Makes more proteins – especially
tubulin for microtubules
• Membrane materials stored in
vesicles under the cell membrane
• DNA winds tightly around proteins to
start mitosis
• Interphase ends
Karyokinesis ( aka
mitosis hyperlink);
M phase)
Equal distribution
of replicated
genetic material
(chromosomes).
Nucleus actively
dividing
(hyperlink)
See mitotic
spindle (diagram
pg 141)
Participants in Mitosis
 Centromere

chromatids
– link sister
Participants, cont

2 identical copies of
chromosomes (sister
chromatids)
Participants, cont
 Spindle
grows from the centrosome/centrioles
 Proteins around the centriole initiate spindle
growth
Mitosis Phases - hyperlink
Prophase (hyperlink)
• DNA coils tightly around proteins
• replicated chromosomes
condense
• centrosomes separate & migrate
toward opposite sides of cell
• mitotic spindle forms
(microtubules grow out from
centrosomes)
• nucleolus disappears
Prometaphase
•
•
nuclear membrane
breaks down- into
small pieces and lay
parallel to the cell
membrane
spindle fibers
attach to
centromeres of
chromosomes
Metaphase
• chromosomes are lined up
single-file along equator of
mitotic spindle.
• Chromosomes seem
motionless because they are
pulled equally by both sides
of the cell
•
Anaphase
•
•
Centromeres, one
per chromatid, move
apart separating
the chromatids to
opposite
Microtubules in the
spindle shorten and
some lengthen in a
way that moves the
poles farther apart
•
Telophase
•
•
•
•
•
•
Cell begins to look like a
dumbell (cytokinesis has
begun)
mitotic spindle breaks
down
chromosomes
decondense
nuclear membranes
reform around two
nuclei
nucleoli reappear
End of Mitosis
3. Cytokinesis
Distribution of cytoplasm and all other
contents to daughter cells.
• begins during anaphase or telophase
depending on the cell type
• differs in animal & plant cells
Cytokinesis in animal cells:
• cleavage furrow (hyperlink)(slight indentation)
forms around equator of cell.
• Contractile ring of actin & myosin microfilaments
act like a drawstring to pinch the cell in two.
• Asters determine the number of cleavage furrows
• usually an equal division.
Cytokinesis in
animal cells
Cytokinesis in plant cells hyperlink:
New cell wall must be built
• phragmoplast (microtubule structure) forms in
cytoplasm & traps vesicles containing cell wall
material. (between daughter cells)
• vesicles fuse, forming a cell plate across midline
of cell.
• cell plate gives rise to two primary cell walls.
Does cytokinesis always accompany
karyokinesis?
Karyokinesis in the absence of cytokinesis
results in a syncytium (mass of multinucleated
cells).
Control of the Cell Cycle hyperlink( what
turns mitosis on or off)
Checkpoints - groups of interacting proteins
that ensure cell cycle events occur in the
correct sequence.
Survivins override
signals that tell the cell
to die, keeping it in
mitosis, not apoptosis
Telomeres
At tip of
chromosomes
 100’s-1000’s of
repeating sequences
on end of chromosome
 Each time mitosis
occurs, DNA looses
50-100 sequences
 After 50+ divisions
DNA signals cell
division to cease

Telomere, con’t



A few cells, DNA does
NOT shrink (bone
marrow, small
intestine, blood cells,
germ cells for sperm)
If DNA shrinks, no
telomerase made
 Telomerase add
DNA to tips of
chromosome
Plant cells produce
telomerase and divide
more than 50 times
Shortening of telomeres - loss of telomere
DNA signals cell to stop dividing.
Some cells produce telomerase (enzyme
that continually adds telomere DNA).
Signals to Divide: Signals from outside the cell
effect cell cycles

Contact Inhibition - healthy cells stop dividing
when they come in contact with other cells.
Signals to Divide, con’t
Hormones - stimulate cell division.
Ex. Estrogen stimulates uterine cell division
Growth factors - proteins that stimulate local
cell division.
Ex. Epidermal growth factor (EGF) stimulates
epithelial cell division filling in new skin
underneath a scab
Ex. Produced in salivary glands of animals –
aids in wound healing
Interaction of kinases & cyclins - activate
genes that stimulate cell division.
Control at the Tissue level – stem cells and cell populations
Stem Cells (hyperlink)
• Cells used to replenish tissues
Stem cell’s con’t
When a stem cell divides,
one daughter cell will
specialize and the other
daughter cell will remain a
stem cell
Ex: basal layer of skin, bone
marrow, & small intestine,
heart and ventricles of
brain
Cell populations – up to 3%
are dividing. (expanding
population) or if all are
dividing it is called a
renewel population
Static populations- cells are
no longer dividing in the
tissue- nerves and muscles
(these enlarge-not divide)
•
Cell death is part of life
B.
Apoptosis (hyperlink)
Programmed cell
death; part of normal
development.
Eliminates excess cells
and cells that could
grow uncontrollably.
Tadpole tail, webbing
between fingers)
Steps of Apoptosis:
Apoptosis












rapidly and neatly dismantle cell into membrane
bound pieces that phagocyte will mop up
(as opposed to necrosis due to injury
death receoptor receives signal
caspases (enzymes that snip cell components) are
activated within
caspases destroy proteins and other components.
caspases destroy adhesion molecules so cell can’t
cling to another cell
cell undulates, forming bulges called blebs
nucleus bursts releasing chromatin
cell shatters
loose membrane surrounds pieces
phagocytes mop up
Similar in plant cells, but parts are digested by
enzymes
Why cells die
Brain cell example pg. 158
 To distinguish self from non-self
 protective function-to detect and
weed out cells that could grow
uncontrollably

C. Cancer (loss of cell cycle control)
Condition resulting from excess cell
division or deficient apoptosis.
Characteristics of Cancer Cells:
•
•
•
•
•
•
•
•
can divide uncontrollably & eternally
dedifferentiation
are invasive
are heritable & transplantable
lack contact inhibition
readily metastasize
exhibit angiogenesis
exhibit genetic mutability









Cancer (hyperlink)- con’t
given nutrients and space, cancer cells reproduce
uncontrollably
growth rate depends on the type of cell
fast growing must be 1 centimeter in diameter- may produce
1 million new cells/hour
loss of cell cycle control is inherited by descendents
injectable
lack contact adhesion
often undergo mutations
stimulate angiogenesis
(blood vessel growth)
Causes of Cancer:
 mistimed or misplaced mitosis
 Absence of normal apotosis (hyperlink)
 Over-expression of oncogenes
 Oncogenes are genes that trigger limited cell division.
 Inactivation of tumor suppressor gene
 Tumor suppressor genes prevent a cell from dividing or
promote apoptosis.
Normal functioning of oncogenes & tumor
suppressor genes may be affected by
environmental factors:
• carcinogens
• radiation
• viruses
• diet
• exercise habits