Transcript File - AP BIOLOGY-

Signals and Cancer
• http://learn.genetics.utah.edu/content/cells
/signals/
1) Look at your
photosynthesis data
-WHAT does it mean?
-WHY did that happen?
-Future experiments?
2) Look at your packet, what
are two ways to graph the
data? What is E50?
Graph and calculate the rate
Warm Up: Solve
using chi-square
Show work
2.71
df/pr
ob.
0.99
0.95
0.90
0.80
0.70
0.50
0.30
0.20
0.10
0.05
1
0.000
13
0.003
9
0.016
0.64
0.15
0.46
1.07
1.64
2.71
3.84
2
0.02
0.10
0.21
0.45
0.71
1.39
2.41
3.22
4.60
5.99
3
0.12
0.35
0.58
1.00
1.42
2.37
3.66
4.64
6.25
7.82
4
0.3
0.71
1.06
1.65
2.20
3.36
4.88
5.99
7.78
9.49
Announcements
• Last days to get stamps on 2A to get FRQ
graded
• Chapters 12-13 reading notes due this
week
• Photosynthesis lab due March 1
onion root tip—slides are the control,
handout is treated with caffeine
Control
Trial
Interphase
Prophase Metaphase
Anaphase
Telophase
1
2
Hypothesis: If we look at a 100 cells then________________________
Caffeine
Trial
Interphase
Prophase Metaphase
Anaphase
Telophase
1
Null Hypothesis: If we compare an onion grown normally and in caffeine
then________________________
Agenda
• Finish mitosis lab counting
• Calculate chi squared for lab—can you
accept null?
• Cell Cycle Coloring with Checkpoints (on
stamp sheet)
• DNA Replication presentation prep (on
stamp sheet)
External signals
• Growth factors
– coordination between cells
– protein signals released by body
cells that stimulate other cells to
divide
• density-dependent inhibition
– crowded cells stop dividing
– each cell binds a bit of growth factor
» not enough activator left to trigger
division in any one cell
• anchorage dependence
– to divide cells must be attached to a
substrate
» “touch sensor” receptors
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
• example: p53
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 is the
Cell Cycle
Enforcer
• 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
p53 discovered at Stony Brook by Dr. Arnold Levine
p53 — master regulator gene
NORMAL p53
p53 allows cells
with repaired
DNA to divide.
p53
protein
DNA repair enzyme
p53
protein
Step 1
Step 2
Step 3
DNA damage is caused
by heat, radiation, or
chemicals.
Cell division stops, and
p53 triggers enzymes to
repair damaged region.
p53 triggers the destruction
of cells damaged beyond
repair.
ABNORMAL p53
abnormal
p53 protein
Step 1
Step 2
DNA damage is
caused by heat,
radiation, or
chemicals.
The p53 protein fails to stop
cell division and repair DNA.
Cell divides without repair to
damaged DNA.
Step 3
cancer
cell
Damaged cells continue to divide.
If other damage accumulates, the
cell can turn cancerous.
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 an
out-of-control
car with many
systems failing!
What causes these “hits”?
• Mutations in cells can be triggered by




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 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
Cancer: breast
cancer cell & mammogram
Traditional treatments for
cancers
• Treatments target rapidly dividing cells
– high-energy radiation
• kills rapidly dividing cells
– chemotherapy
• stop DNA replication
• stop mitosis & cytokinesis
• stop blood vessel growth
New “miracle drugs”
• Drugs targeting proteins (enzymes) found
only in cancer cells
– Gleevec
• treatment for adult leukemia (CML)
& stomach cancer (GIST)
• 1st successful drug targeting only cancer cells
without
Gleevec
Novartes
with
Gleevec
The mitotic spindle at metaphase
•Each of the two joined chromatids of
a chromosome has a kinetochore.
•Anaphase: proteins holding together
the sister chromatids of each
chromosome are inactivated and
they are now full chromosomes.
•Experimental evidence supports
the hypothesis that kinetochores
use motor proteins that "walk" a
chromosome along the attached
microtubules toward the nearest
pole.
•Meanwhile, the microtubules
shorten by depolymerizing at
their kinetochore ends
•In a dividing animal cell,
non kinetochore microtubules are
responsible for elongating the
whole cell during anaphase
Chromosome movement
• Kinetochores use
motor proteins that
“walk” chromosome
along attached
microtubule
– microtubule shortens
by dismantling at
kinetochore
(chromosome) end
Look at the steps of mitosis
Book pgs 210-211
Write and draw what happens
in each part of mitosis
How is cytokinesis different in
plants and animal? Page 214
10 minutes
Announcements
• Last days to get stamps on 2A to get FRQ
graded
• Chapters 12-13 reading notes due this
week
• Photosynthesis lab due March 1
• Sub Friday—a friend so be good 
• Thanks for the b-day poster period 4 
Team Whiteboard
•
•
•
•
•
•
Cytokinesis in Animals
Metaphase
Cytokinesis in Plants
Prophase
Anaphase
Telophase
The Cell Cycle Clock: Cyclins and Cyclin-Dependent Kinase
•Fluctuations in the abundance and activity of cell cycle control molecules pace
the sequential events of the cell cycle.
•Protein kinases, give the go-ahead signals at the G1 and G2 checkpoints
•The kinases are present at a constant concentration in the growing cell, but
much of the time they are in inactive form.
•To be active, such a kinase must be attached to a cyclin, a protein that gets its
name from its cyclically fluctuating concentration in the cell.
•These kinases are called cyclin-dependent kinases, or Cdks. The activity of a
Cdk rises and falls with changes in the concentration of its cyclin partner.
Cdks are relatively
constant
Cyclins vary in the
cycle
The stages of mitotic cell division in an animal cell
The light micrographs show dividing lung cells from a newt, which has 22
chromosomes in its somatic cells. The chromosomes appear blue and the
microtubules green. (Know the characteristics of the phases)
Review the details of each mitotic phase animal cells
(Know the characteristics of the phases)
Mitosis flash animation (Purves)
Cytokinesis divides the cytoplasm
How does it differ in animal and plant cells?
In animal cells, cytokinesis occurs by cleavage
•The cleavage furrow, which begins as a shallow groove in the cell
surface.
• On the cytoplasmic side, a contractile ring of actin microfilaments
and molecules of the protein myosin
•The contraction of the dividing cell’s ring of microfilaments is like the
pulling of drawstrings
Cytokinesis animation
Cytokinesis
• Cytoplasmic division
• Animals
– constriction belt of
actin microfilaments
around equator of
cell
• cleavage furrow
forms
• splits cell in two
• like tightening a draw
string
Cytokinesis in Plants
• Plants
– cell plate forms
• vesicles line up at
equator
– derived from Golgi
• vesicles fuse to form 2
cell membranes
– new cell wall laid
down between
membranes
• new cell wall fuses with
existing cell wall
Going to calculate statistically if
a phase is overrepresented
• Chi-squared
Statistical Test
• We want to determine if a coin is fair. In other words, are
the odds of flipping the coin heads-up the same as tailsup.
• We collect data by flipping the coin 200 times. The coin
landed heads-up 108 times and tails-up 92 times.
• At first glance, we might suspect that the coin is biased
because heads resulted more often than tails.
• To analyze our results use a chi-squared test.
• "The null hypothesis in a chi-square
goodness-of-fit test states that the sample of
observed frequencies supports the claim
about the expected frequencies.
• The alternative hypothesis states that there
is no support for the claim pertaining to the
expected frequencies."
• Null hypothesis--The coin should be
equally likely to land head-up or tails-up
every time
• Alternate Hypothesis— The coin is
rigged and will not land equally on heads
or tails
Heads
Tails
Total
Observed
108
92
200
Expected
100
100
200
Total
The next step is to prepare a table as follows.
208
192
400
Chi-squared =
(108-100)2/100 + (92-100) 2/100 =
(8) 2/100 + (-8) 2/100 =
0.64 + 0.64 = 1.28
Bio
uses
0.05
df/pr
ob.
0.99
0.95
0.90
0.80
0.70
0.50
0.30
0.20
0.10
0.05
1
0.000
13
0.003
9
0.016
0.64
0.15
0.46
1.07
1.64
2.71
3.84
2
0.02
0.10
0.21
0.45
0.71
1.39
2.41
3.22
4.60
5.99
3
0.12
0.35
0.58
1.00
1.42
2.37
3.66
4.64
6.25
7.82
4
0.3
0.71
1.06
1.65
2.20
3.36
4.88
5.99
7.78
9.49
5
0.55
1.14
1.61
2.34
3.00
4.35
6.06
7.29
9.24
11.07
Degrees of freedom by subtracting one from the number of classes.
In this example, we have two classes (heads and tails), so our degrees of
freedom is 1.
Our chi-squared value is 1.28.
Because the chi-squared value we obtained in the coin example is greater than
0.05, we accept the null hypothesis as true and conclude that our coin is fair.
So for mitosis lab
• Create null hypothesis about cells treated
with caffeine vs not treated with caffeine
Interpret diagram from notes or
book pg 209
THE MITOTIC CELL
CYCLE
The mitotic phase
alternates with interphase
in the cell cycle
What are the key
parts of each
phase?
Mitosis animation
How does
our body
regulate the
cell cycle?
Cell Cycle regulation
• Checkpoints
– cell cycle controlled
by STOP & GO
chemical signals at
critical points
– signals indicate if
key cellular
processes have
been
completed correctly
Checkpoint control system
• 3 major checkpoints:
– G1/S
• can DNA synthesis begin?
– G2/M
• has DNA synthesis been
completed correctly?
• commitment to mitosis
– spindle checkpoint
• are all chromosomes attached
to spindle?
• can sister chromatids separate
correctly?
G1/S checkpoint
• G1/S checkpoint is most critical
– primary decision point
• “restriction point”
– if cell receives “GO” signal, it divides
• internal signals: cell growth (size), cell nutrition
• external signals: “growth factors”
– if cell does not receive
signal, it exits cycle &
switches to G0 phase
• non-dividing, working state
“Go-ahead” signals
• Protein signals that promote cell growth
& division
– internal signals
• “promoting factors”
– external signals
• “growth factors”
• Primary mechanism of control
– phosphorylation
• kinase enzymes
• either activates or inactivates cell signals
inactivated Cdk
Cell cycle signals
• Cell cycle controls
– cyclins
• regulatory proteins
• levels cycle in the cell
– Cdks
• cyclin-dependent kinases
• phosphorylates cellular proteins
activated Cdk
– activates or inactivates proteins
– Cdk-cyclin complex
• triggers passage through different stages of
cell cycle
Meiosis
Bring your grade up. Put in the time to read, come
into office hours, ASK questions
Dispatch: In YOUR OWN words contrast…
a) somatic vs gamete
b) diploid vs haploid
c) homologous chromosome vs chromosome
d) meiosis vs mitosis
e) chromatid vs chromosome
f) allopatric vs sympatric
g) depolarization vs polarization
h) Meiosis part I vs Meiosis part II
i) Evolution vs Hardy-Weinberg
• Evolution is one of the unifying themes of biology.
Evolution involves change in the frequencies of alleles in
a population. For a particular genetic locus in a
population, the frequency of the recessive allele (a) is
0.4 and the frequency of the dominant allele (A) is 0.6.
(a) What is the frequency of each genotype (AA, Aa, aa) in
this population? What is the frequency of the dominant
phenotype?
(b) How can the Hardy-Weinberg principle of genetic
equilibrium be used to determine whether this population
is evolving?
(c) Identify a particular environmental change and describe
how it might alter allelic frequencies in this population.
Explain which condition of the Hardy-Weinberg principle
would not be met.
Battle
•
•
•
•
•
Metaphase I
Metaphase II
Prophase I
Anaphase II
Anaphase I
Seat 1
•Metaphase I
Seat 2
•Anaphase I
Seat 3
• Metaphase II
Seat 4
• Prophase I
Any seat
• Anaphase II
Dispatch
1) What are microtubules?
2) What is the role of microtubules in cell
division?
3) Draw a cell in Metphase I and label
-centrioles
-microtubules
-chromosomes
Pick up study guide
• Answer using only your reading notes
What do you know about
cytoskeleton?
Role of cytoskeleton
• http://www.youtube.com/watch?v=5rqbmLiS
kpk&feature=related
• http://bio.rutgers.edu/~gb101/lab2_mitosis/s
ection2_frames.html
The mitotic spindle distributes chromosomes to daughter
cells
The assembly of spindle microtubules starts in the centrosome, known as a
microtubule-organizing center.
During interphase, the single centrosome replicates to form two centrosomes.
During prophase they form spindle fibers and migrate to the poles.
Show the movement of
chromosomes
-Polar microtubules
-Kinetochore microtubules
5 min
NEXT FRQ: The role of 3 proteins in cell
cycle
• http://highered.mcgrawhill.com/olcweb/cgi/pluginpop.cgi?it=swf::5
35::535::/sites/dl/free/0072437316/120073
/bio14.swf::Mitosis%20and%20Cytokinesis
Crossing over comic
•
Show homologous pairs crossing over to
contribute to variation
•
Make it funny
•
Underneath give the academic definition with
the terms
1) Crossing over
2) Homologous chromosomes
3) Variation
4) Prophase I of meiosis
Somatic Cells:
•body cells
•Ex. ___________
•Made by mitosis
Gametes:
•reproductive cells
•Ex. ________
Diploid:
•Having 2 copies of each
chromosome (2n), one from each
parent
•Somatic cells are diploid
•Human diploid number is _____
Haploid:
•Having only 1 copy of each
chromosome (n)
•Gamete cells are haploid
•Human haploid number is _____
What are the cells in your body that
are haploid?
Copy and fill in the chart below.
Organism
Diploid # (in somatic Haploid # (in
cells)
gametes)
Cat
Rose
19
12
Goat
Rice
30
24
Dog
Chimpanzee
39
48
• http://www.wiley.com/college/boyer/04700
03790/animations/protein_folding/protein_f
olding.htm
THE CELL CYCLE: Chapter 12
Without counting the G 0 phase, a cell cycle takes 12-24
hours for most mammalian cells, and only 20-30
minutes for E. coli cells
• http://highered.mcgrawhill.com/sites/0072495855/student_view0/ch
apter2/animation__how_the_cell_cycle_wor
ks.html
• Take notes on events of each part of the cell
cycle
• Interphase (G1, S, G2) + PMATC
• Follow alleles
Get a whiteboard and beads
• Every eukaryotic species has a
characteristic number of chromosomes in
each cell nucleus
• Somatic (nonreproductive) cells have two
sets of chromosomes
• Gametes (reproductive cells: sperm and
eggs) have half as many chromosomes as
somatic cells
• Eukaryotic chromosomes consist of
chromatin, a complex of DNA and protein
that condenses during cell division
Dispatch
• Our DNA is 6 feet long, how does it fit into
a nucleus? Note: 10,000 nuclei fit on the
tip of your pencil. Hint on pg 320-321 or
345
• http://dnalc.org/view/15491-DNApackaging-3D-animation-withnarration.html
Chromosome duplication and
distribution during mitosis.
Eukaryotic duplicates each of its
multiple chromosomes before it
divides.
A duplicated chromosome
consists of two sister
chromatids, which narrow at
their centromeres.
Cytokinesis in plant cells has no cleavage furrow
During telophase, vesicles derived from the Golgi apparatus move along
microtubules to the middle of the cell, where they fuse, producing a cell
plate.
Mitosis in a plant cell
These light micrographs show mitosis in cells of an onion root.
How does this differ from animal cell mitosis?
Mitosis in eukaryotes may have
evolved from binary fission in
bacteria
Mitosis video (long)
A hypothesis for the
evolution of mitosis
Researchers of eukaryotic
cell division have
observed in modern
organisms what they
believe are mechanisms
of division intermediate
between the binary fission
of bacteria and mitosis as
it occurs in most
eukaryotes.
Cancer
This man has cancer of the mouth.
Regulation of the Cell cycle
The timing and rate of cell division in different parts of a plant or animal
are crucial to normal growth, development, and maintenance.
Do all cells have the same cell cycle?
Why is regulation of the cell cycle of interest to research?
Cancer Growth Flash animation
What is Cancer?
• Cancer means
uncontrolled cell growth
• The body needs to keep
cell growth = cell death
• Cell cycle checkpoints kill
mutated or old cells
• http://science.education.nih.gov/supplement
s/nih1/cancer/activities/activity2_animations.
htm
The cell cycle has traffic lights that serve as checkpoints
G1 Phase
S Phase
G2 Phase
Does the body
need more
cells?
Is the cell ready for mitosis?
Cancer is caused when the checkpoints are broken
and the cell cycle keeps going without stopping
G1 Phase
S Phase
G2 Phase
What are the types of cancer?
*Any part of the body can be cancerous
• Skin cancer
• Lung cancer
• Breast cancer
• Testicular cancer
• Colon cancer
• Liver cancer
• Brain cancer
Lung
Cancer
Brain
Cancer
How do you get cancer?
How can you get cancer?
• Getting hit in the breast?
NO
• Having unprotected sex?
NO
• Smoking?
YES
• Being in the sun too long?
YES
Why
is
cancer
so
deadly?
1) Mutated cells beat the cell
cycle checkpoints and keep
dividing
2) They form tumors which
then stop your body parts
from functioning normally
3) Angiogensis – the tumors
hijack blood vessels to keep
them alive
4) Metastisis – the cells from
the tumor travel and infect
other parts of your body
*
Here is the development of colon cancer.
Why is Cancer so Hard to Cure?
1) It is a silent killer, by the
time it is found it is
already to late
2) Chemo/Radiation
therapy can kill cancer
cells, but is hard on
patients
3) If one cancer cell
survives, or travels,
cancer will come back
Can cancer be prevented?
Cancer is not contagious.
There is no guaranteed way to prevent cancer,
people can reduce their risk (chance) of
developing cancer by:
A) not using tobacco products
B) choosing foods with less fat and eating more
vegetables, fruits, and whole grains
C) exercising regularly and maintaining a lean weight
D) avoiding the harmful rays of the sun, using
sunblock, and wearing clothing that protects the
skin
Mechanical analogy for the cell cycle control system
In this diagram of the cell cycle, the flat "stepping stones" around the
perimeter represent sequential events. Like the control device of an
automatic washer.
Cell Cycle Checkpoints
•A checkpoint is a critical control point where stop and go-ahead signals
can regulate the cycle.
•The G1 checkpoint (the "restriction point”) is most important.
•If a cell receives a go-ahead signal at the G1 checkpoint, it will usually
complete the cycle and divide.
•If it does not receive a go-ahead signal at that point, it will exit the
cycle, switching into a non-dividing state called the G0 phase.
G0 (G zero)
resting phase
Cell Cycle with Checkpoints
Animation
Many factors are involved in the regulation of the cell cycle
RB inhibits cell division
Active Cdk inhibits RB
Cdks are relatively constant
Cyclins vary in the cycle
The active enzyme and the activating process can be inhibited by two
families of cell cycle inhibitory proteins.
1. Members of the INK4 family bind free CDKs thereby preventing
association with cyclins.
2. Members of the CIP family bind and inhibit the active CDK-cyclin
complex.
http://www.chemsoc.org/exemplarchem/entries/2001/armour/howstrt.htm
Internal and external cues help regulate the cell cycle
Internal Signals: Messages from the Kinetochores: the APC
A gatekeeper at the M phase checkpoint delays anaphase. Regulators from
kinetochores insures all the chromosomes are properly attached to the spindle
at the metaphase plate and the anaphase-promoting complex (APC) is in an
inactive state. When all are attached, the APC then becomes active and
indirectly triggers both the breakdown of cyclin and the inactivation of proteins
holding the sister chromatids together.
Degradation of key regulator
proteins such as the anaphase
inhibitors PDS1 and CUT2, and
the mitosis initiator cyclin B,
drives the cell cycle forward.
Molecular control of the cell cycle
at the G2 checkpoint.
The Cdk-cyclin complex called MPF,
which acts at the G2 checkpoint to
trigger mitosis.
The "maturation-promoting factor"
triggers the cell’s passage past the G2
checkpoint into M phase
Cyclins accumulate during G2
associate with Cdk molecules, the
resulting MPF complex initiates
mitosis.
Later in the M phase, MPF helps
switch itself off by initiating a process
that leads to the destruction of its
cyclin by a protein breakdown
mechanism
Ubiquitin is part of the pathway for the degradation of proteins
Ubiquitin is part of the pathway for the degradation of proteins
External Signals: Growth Factors
One example of a growth factor is platelet-derived growth factor
(PDGF), which is made by blood cells called platelets.
The binding of PDGF molecules to these receptors triggers a signaltransduction pathway that leads to stimulation of cell division.
The proliferation of fibroblasts helps heal the wounds.
Density-dependent
inhibition of cell division.
Most animal cells also exhibit
anchorage dependence
Cancer cells exhibit neither
density-dependent inhibition
nor anchorage dependence
Cancer cells have escaped from cell cycle controls
Cancer cells do not respond normally to the body’s control mechanisms.
They divide excessively and invade other tissues. If unchecked, they
can kill the organism.
The growth and metastasis of a malignant breast tumor.
What is a benign tumor? A malignant tumor? metastasis
Breast cancer animation
P53 is considered to be a "Guardian of the Genome“
1. Growth arrest: p21, Gadd45, and 14-3-3s.
2. DNA repair: p53R2.
3. Apoptosis: Bax, Apaf-1, PUMA and NoxA.
P53 re-enforces the G2 checkpoint. This serves as a “tumor
suppressor” protein.
In the cell, p53 protein binds DNA, which in turn stimulates another gene to
produce a protein called p21 that interacts with a cell division-stimulating
protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass
through to the next stage of cell division. Mutant p53 can no longer bind
DNA in an effective way, and as a consequence the p21 protein is not made
available to act as the 'stop signal' for cell division. Thus cells divide
uncontrollably, and form tumors.
http://highered.mcgrawhill.com/sites/007337797x/student_view
0/chapter9/animation_quiz__how_tumor_suppressor_genes_block_
cell_division.html
•Explain the
following diagram
Mitosis vs. Meiosis
Meiosis
Somatic Cells:
•body cells
•Ex. ___________
•Made by mitosis
Gametes:
•reproductive cells
•Ex. ________
Diploid:
•Having 2 copies of each chromosome (2n), one
from each parent
•Somatic cells are diploid
•Human diploid number is _____
What are the cells in your body that are diploid?
Are gametes diploid? Why or why not?
How many chromosomes does a sperm and egg
have?
Haploid:
•Having only 1 copy of each chromosome (n)
•Gamete cells are haploid
•Human haploid number is _____
What are the cells in your body that are haploid?
Copy and fill in the chart below.
Organism
Diploid # (in somatic Haploid # (in
cells)
gametes)
Cat
Rose
19
12
Goat
Rice
30
24
Dog
Chimpanzee
39
48
Homologous pair:
•A pair of chromosomes, 1 from mom and 1 from
dad
•Carry the same genes (ex. eye color gene)
•But may contain different information (ex. brown
eyes and blue eyes)
Eye color gene
Mitosis:
How our bodies make diploid somatic cells
It happens ________________
Meiosis:
The special process of making haploid gametes
It happens in the ______________ & ______________
Do you do mitosis?
Do you do meiosis?
Meiosis Video 1
Mitosis vs. Meiosis Video
Meiosis
Homologous Chromosomes are
Homies
• They are always the same SIZE
• They always have the same type of INFO,
but they are not identical
Whiteboard Games
1) All members help to find the answer
2) There will be a seat number who will write
and a seat number who will present
Game 1: Whose my Homie?
Seat 2—
Writes
Seat 3-Present
s
#1
#2
#3
#4
#6
#5
Activity
• Make 1 set of homologous pairs of
chromosomes=2 chromosomes
• Put letters on the chromosomes
• Demonstrate crossing over
• Tips: Use whiteboard and move beads
Game 2: Crossing Over
• On page 90 all members need to draw
crossing over between homologous
chromosomes IN COLOR
• Book pg 276
Drawing 1—2 homologous chromosomes with
letters
Drawing 2—Crossing over (twisty style)
Drawing 3—Final chromosomes
On the bottom of page 90 write
• Crossing over occurs between
homologous chromosomes
• This only occurs in MEIOSIS
• Crossing over occurs during prophase 1
and leads to different sperm and egg
Dispatch pg 93
• Crossing over is when________________
• Crossing over occurs during____phase of
meiosis
Mendel’s 2 Laws
Independent Assortment
• http://www.sumanasinc.com/webcontent/a
nimations/content/independentassortment.
html
On pg 91 write
• Mendel’s Law of Independent
Assortment— homologous chromosomes
line up in different combinations during
Metaphase I of Meiosis
Draw 2
different
alignments
Game 3: 2 alignments for these 2
homies
E
j
e
J
Mendel’s Law 2 pg 92
• Mendel’s Law of Segregation —allele pairs
separate during gamete formation and end
up in different gametes (sperm and egg)
Draw 4 sperm
that are
segregated
Game 4: Segregation or Not?
Seat 4—
Writes
Seat 1-Present
s
#1
#2
#3
#4
Who won?
• Clean up beads, colored pencils, marker
and whiteboard
• Get ready for exit quiz
Exit Quiz
1)Draw a sperm cell that is
segregated
2)Draw 2 alignments for
homologous chromosomes
in metaphase 1
Exit Quiz
1) Explain how the cell cycle is regulated
2) How does cancer occur?
3) Give 5 differences between mitosis and
meiosis
Chapter 12~
The Cell Cycle
Biology is the only subject in
which multiplication is the same
thing as division…
2007-2008
Why do cells divide?
• For reproduction
– asexual reproduction
• one-celled organisms
• For growth
– from fertilized egg to
multi-celled organism
amoeba
• For repair & renewal
– replace cells that die
from normal wear & tear
or from injury
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Importance of Cell Division
1. Growth and Development
Zygote
1 Cell
Embryo
100 cells
2. Asexual Reproduction
Fetus
millions cells
Adult
100 trillion cells
3. Tissue Renewal
DNA organization in Prokaryotes
• Nucleoid region
• Bacterial Chromosome
– Single (1) circular DNA
– Small
• (e.g. E. coli is 4.6X106 bp, ~1/100th human
chromosome)
• Plasmids – extra chromosomal DNA
Bacterial Fission
The Cell Cycle
• Interphase (90% of cycle)
• G1 phase~ growth
• S phase~ synthesis of DNA
• G2 phase~ preparation for
cell division
• Mitotic phase
• • Mitosis~ nuclear division
• • Cytokinesis~ cytoplasm
division
Parts of Cell Cycle
• Interphase
– G1
– S phase
– G2
• M phase
– Mitosis (Division of nucleus)
•
•
•
•
•
Prophase
Prometaphase
Metaphase
Anaphase
Telophase
– Cytokinesis (Division of
cytoplasm)
Cell Division: Key Roles
•
•
•
•
•
•
•
•
•
•
•
•
Genome: cell’s genetic
information
Somatic (body cells) cells
Gametes (reproductive cells):
sperm and egg cells
Chromosomes: condensed DNA
molecules
Diploid (2n): 2 sets of
chromosomes
Haploid (1n): 1 set of
chromosomes
Chromatin: DNA-protein
complex
Chromatids: replicated strands
of a chromosome
Centromere: narrowing “waist”
of sister chromatids
Mitosis: nuclear division
Cytokinesis: cytoplasm division
Meiosis: gamete cell division
Chromosome Organization
• When cells divide, daughter cells must each
receive complete copy of DNA
• Each cell has about 2 meters of DNA in the
nucleus; thin threads called chromatin
• Before division, condenses to form
chromosomes
• DNA also replicates before cell division to
produce paired chromatids
156
doublestranded
mitotic human
chromosomes
Normal Karyotype (Fig 18.1)
158
Mitosis
•
•
•
•
•
Prophase
Prometaphase
Metaphase
Anaphase
Telophase
Prophase
• Chromatin condenses
– visible chromosomes
• chromatids
• Centrioles move to opposite
poles of cell
– animal cell
• Protein fibers cross cell to
form mitotic spindle
– microtubules
• Nucleolus disappears
• Nuclear membrane breaks
down
Prometaphase
– spindle fibers attach to
centromeres
• creating kinetochores
– microtubules attach at
kinetochores
• connect centromeres to
centrioles
– chromosomes begin
moving
Metaphase
• Centrosomes at
opposite poles
• Centromeres are
aligned
• Kinetochores of sister
chromatids attached
to microtubules
(spindle)
Anaphase
• Paired centromeres
separate; sister
chromatids liberated
• Chromosomes move
to opposite poles
• Each pole now has a
complete set of
chromosomes
Separation of chromatids
• In anaphase, proteins holding together sister
chromatids are inactivated
– separate to become individual chromosomes
1 chromosome
2 chromatids
double-stranded
2 chromosomes
single-stranded
Telophase
• Daughter nuclei form
• Nuclear envelopes
arise
• Chromatin becomes
less coiled
• Two new nuclei
complete mitosis
• Cytokinesis begins
– cell division
Mitosis in whitefish blastula
Mitosis in plant cell
Any Questions??