Cell Cycle, Mitosis,
Meiosis
Unit 5
 Musical Chairs
 TODAY:
Welcome
Back!
 Notes on Cell Cycle
 Become medical school students on oncology rotation
 Homework for next time: Watch Bozeman video on cell cycle,
mitosis and meiosis. There *may* be a quiz.
 AP Biology Essential Knowledge covered:
In eukaryotes, heritable information is passed to the next
generation via processes that include the cell cycle and mitosis or
meiosis plus fertilization.
Unit 5 Plan
 Day 1 – Cell Cycle & Case Study
 Day 2 – Mitosis & Case Study
 Day 3 – Meiosis & Modeling Activity
 Day 4 – Modeling continued, Quiz over notes/Quizlet (online)
 Lifetime Risk of Developing Cancer: Approximately _____ percent
of men and women will be diagnosed with all cancer sites at some
point during their lifetime?
Why Care about
Cell Cycle
Control?
 In 2012, there were an estimated __________ people living with all
cancer sites in the United States.
Why Care about
Cell Cycle
Control?
 Lifetime Risk of Developing Cancer: Approximately 39.6 percent
of men and women will be diagnosed with all cancer sites at some
point during their lifetime?
 In 2012, there were an estimated 13, 780,000 people living with all
cancer sites in the United States.
Oncologists – Study cancer
and help those affected
 Average salary in 2015 ~ $277,000
Why Care about
Cell Cycle
Control?
Time to become an oncologist?
10-13 years
Bachelors, Medical School, Residency
Demand?
United States will likely face a 48% increase in demand for oncologist
services by 2020—in large part because of the expected 81% increase
in cancer survivorship and the 48% increase in cancer
incidence caused by the aging of the population.
 In eukaryotes, heritable information is passed to the next
generation via processes that include the cell cycle and mitosis or
meiosis plus fertilization.
Day 1 –
Cell Cycle
 So, passing on heritable information begins with the ability for
cells to go through the cell cycle.
 Why else is the cell cycle important?
Some Cell
Cycle Basics
Mitotic Phase
The cell cycle is divided into Interphase and Mitotic (including mitosis & cytokinesis)
Interphase consists of three phases: growth, synthesis of DNA, preparation for mitosis.
Mitosis consists of prophase, metaphase, anaphase and telophase.
Mitosis alternates with interphase in the cell cycle.
Cell division
results in
genetically
identical cells
How do cells know when to divide?
Activation of
cell division
Cell communication signals
 chemical signals in cytoplasm give cue
 signals usually are proteins
 activators
 inhibitors
 A multicellular organism needs to coordinate cell division across
different tissues & organs
 critical for normal growth,
development & maintenance
Coordination
of cell division
Do you think cells all have
the same timing for their
cell cycle?
Discuss with a friend –
think of an example.
 Frequency of cell division varies by cell type
 embryo
 cell cycle < 20 minute
 skin cells
 divide frequently throughout life
 12-24 hours cycle
Frequency of
cell division
 liver cells
 retain ability to divide, but keep it in reserve
 divide once every year or two
M
metaphase anaphase
telophase
prophase
 mature nerve cells & muscle cells
C
 do not divide at all after maturity
 permanently in G0
G2
S
interphase (G1, S, G2 phases)
mitosis (M)
cytokinesis (C)
G
1
 The cell cycle is a complex set of stages that is highly regulated
with checkpoints, which determine the ultimate fate of the cell.
Cell Cycle –
Think/Pair/Share
 Why would it need to be highly regulated?
 What might the checkpoints result in?
 Two irreversible points in cell cycle
There’s no
turning back,
now!
 replication of genetic material
 separation of sister chromatids
 Checkpoints
 process is assessed & possibly halted
Overview of
Cell Cycle
Control
centromere
single-stranded
chromosomes
sister chromatids

double-stranded
chromosomes

 Checkpoints
 cell cycle controlled by STOP & GO chemical signals at critical points
 signals indicate if key cellular
processes have been
completed correctly

3 major checkpoints:

Checkpoint
control system
G1, G2 and M
 3 major checkpoints:
 G1
 can DNA synthesis begin?
 G2
 has DNA synthesis been completed correctly?
 commitment to mitosis
 M
Checkpoint
control system
 are all chromosomes attached to spindle?
 can sister chromatids separate correctly?
G1 Checkpoint is
the most critical!
 primary decision point
 “restriction point”
 if cell receives a “GOahead”signal, it will
divide
 if cell does not receive
signal, it exits cycle &
switches to G0 phase
 G0 phase
 non-dividing, differentiated state
 many human cells in G0 phase
G0 phase
 liver cells
 in G0, but can be “called
M
Mitosis
G2
Gap 2
S
Synthesis
G1
Gap 1
G0
Resting
back” to cell cycle by
external cues
 nerve & muscle cells
 highly specialized
 arrested in G0 & can
never divide
Protein molecules that promote cell
growth & division
 internal signals
 “promoting factors”
 external signals
 “growth factors”
“Go-ahead”
signals
 Primary mechanism of control
 phosphorylation
 Use of kinase enzymes
 Which either activates or
inactivates cell signals by
adding a phosphate
 Cyclins (PROTEIN)
 regulatory proteins
 levels cycle in the cell
inactivated Cdk
 Cdk’s (ENZYME)
Cell cycle
Chemical signals
 cyclin-dependent kinases
 phosphorylates cellular
proteins
 activates or inactivates
proteins
 Cdk-cyclin complex
 Forms MPF (mitosis
promoting factor) complex
 Triggers movement into next
phase
activated Cdk
M checkpoint
G2 checkpoint
Chromosomes attached
at metaphase plate
• Replication completed
• DNA integrity
Active
Inactive
Cdk / G2
cyclin (MPF)
Inactive
M
Active
C
cytokinesis
mitosis
G2
G1
S
MPF = Mitosis
Promoting Factor
Cdk / G1
cyclin
Active
G1 checkpoint
Inactive
• Growth factors
• Nutritional state of cell
• Size of cell
Cyclin & Cyclin-dependent kinases (Cdk’s)
 CDKs & cyclin drive cell from
one phase to next in cell cycle

proper 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
(including humans)
Sometimes the signals are EXTERNAL…
Growth factors
 Proteins or steroid hormones that bind to receptors on the
cell surface, with the primary result of activating cellular
proliferation and/or differentiation.
 Many growth factors are quite versatile, stimulating cellular
division in numerous different cell types; while others are
specific to a particular cell-type
External
signals
 Allow coordination between cells
 density-dependent inhibition
 crowded cells stop dividing
 When not enough growth factor left to trigger division in
any one cell, division stops
 anchorage dependence
 to divide cells must be attached to a substrate or tissue
matrix
 “touch sensor” receptors
 Cancer is essentially a failure
of cell division control
 unrestrained, uncontrolled cell growth
 What control is lost?
Cancer & Cell
Growth
p53 is the
Cell Cycle
Enforcer
 lose checkpoint stops
 gene p53 plays a key role in G1 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
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)
Development
of Cancer
 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 an
out of control
car!
Mutations in cells can be triggered by



What causes
these “hits”?

UV radiation
chemical exposure
radiation exposure
heat




cigarette smoke
pollution
age
genetics
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 tumors
 cells leave original site
 carried by blood & lymph system to other tissues
 start more tumors = metastasis
 impair functions of organs throughout body
Treatments target rapidly dividing cells
 high-energy radiation
 kills rapidly dividing cells
 chemotherapy
 stop DNA replication
 stop mitosis & cytokinesis
 stop blood vessel growth
Traditional
treatments for
cancers
 You are medical school students on an oncology rotation
 Choose a narrator, scribe and researcher
Time for your
oncology
rotation!
 Start with the “Mystery” – when you have answered the
questions, raise a hand for your supervisor to check in with you
(yes, that is me)
 You must check in with me before proceeding to each new portion
of your case study.
 Your group’s grades will be based on our discussions – everyone
must be prepared to answer the supervisors questions!