Cell division (Chapter 10) - California Lutheran University

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Cell division
Chapter 10
Genes and Development
Fig. 10.1-1
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Bacterial cell
Origin of
replication
Bacterial chromosome:
Double-stranded DNA
Fig. 10.1
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Bacterial cell
Bacterial chromosome:
Double-stranded DNA
Origin of
replication
Septum
Fig. 10.2
Fig. 10.3a
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Prokaryotes
No nucleus, usually
have single circular
chromosome. After DNA
is replicated, it is
partitioned in the cell.
After cell elongation,
FtsZ protein assembles
into a ring and facilitates
septation and cell
division.
Chromosome
FtsZ protein
Septum
Fig. 10.3
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Prokaryotes
No nucleus, usually
have single circular
chromosome. After DNA
is replicated, it is
partitioned in the cell.
After cell elongation,
FtsZ protein assembles
into a ring and facilitates
septation and cell
division.
Chromosome
Some Protists
Nucleus present and
nuclear envelope
remains intact during
cell division.
Chromosomes line up.
Microtubule fibers pass
through tunnels in the
nuclear membrane and
set up an axis for
separation of
replicated
chromosomes, and cell
division.
FtsZ protein
Microtubule
Chromosome
Other Protists
A spindle of microtubules forms between
two pairs of centrioles at
opposite ends of the
cell. The spindle passes
through one tunnel in
the intact nuclear
envelope. Kinetochore
microtubules form
between kinetochores
on the chromosomes
and the spindle poles
and pull the chromosomes to each pole.
Yeasts
Nuclear envelope
remains intact; spindle
microtubules form inside
the nucleus between
spindle pole bodies. A
single kinetochore
microtubule attaches to
each chromosome and
pulls each to a pole.
Kinetochore microtubule
Animals
Spindle microtubules
begin to form between
centrioles outside of
nucleus. Centrioles move
to the poles and the
nuclear envelope breaks
down. Kinetochore
microtubules attach
kinetochores of
chromosomes to spindle
poles. Polar microtubules
extend toward the center
of the cell and overlap.
Spindle pole body
Kinetochore microtubule
Fragments
of nuclear
envelope
Kinetochore microtubule
Central spindle
of microtubules
Septum
Polar microtubule
Nucleus
Centrioles
Kinetochore
Centriole
Polar microtubule
Table 10.1
Fig. 10.5-1
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Chromosome
Fig. 10.5-2
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Chromosome
Rosettes of Chromatin Loops
Scaffold protein
Fig. 10.5-3
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Chromosome
Rosettes of Chromatin Loops
Scaffold protein
Chromatin Loop
Scaffold
protein
Chromatin loop
Fig. 10.5-4
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Chromosome
Rosettes of Chromatin Loops
Scaffold protein
Chromatin Loop
Scaffold
protein
Chromatin loop
Solenoid
Fig. 10.5
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Chromosome
Rosettes of Chromatin Loops
Scaffold protein
Chromatin Loop
Solenoid
Scaffold
protein
Chromatin loop
DNA Double Helix (duplex)
Nucleosome
Histone core
DNA
Animation of DNA coiling
DNA coiling and cells dividing
Fig. 10.6
Fig. 10.7
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Homologous chromosomes
Homologous chromosomes
Kinetochore
Replication
Cohesin
proteins
Centromere
Kinetochores
Sister chromatids
Sister chromatids
Fig. 10.8
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M Phase
Metaphase
Anaphase
Prometaphase
Telophase
Prophase
G2
G1
S
Interphase
G2
Mitosis
M Phase
Cytokinesis
S
Cell cycle
G1
Fig. 10.9
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Cohesin
proteins
Chromatid
Centromere
region of
chromosome
Kinetochore
Kinetochore
microtubules
Metaphase
chromosome
Fig. 10.10
Red = Cohesin
Green = Kinetochore
Blue = Chromosome
Fig. 10.11a
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INTERPHASE G2
Centrioles
(replicated;
animal
cells only)
80 µm
Chromatin
(replicated)
Aster
Nuclear
membrane
Nucleolus
Nucleus
• DN A has been replicated
• Centrioles replicate (animal cells)
• Cell prepares for division
© Andrew S. Bajer, University of Oregon
Fig. 10.11b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
MITOSIS
Prophase
80 µm
Mitotic spindle
beginning to form
Condensed
chromosomes
• Chromosomes condense and
become visible
• Chromosomes appear as two
sister chromatids held together
at the centromere
• Cytoskeleton is disassembled:
spindle begins to form
• Golgi and ER are dispersed
• Nuclear envelope breaks down
© Andrew S. Bajer, University of Oregon
Fig. 10.11c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
MITOSIS
Prometaphase
80 µm
Centromere and Mitotic
kinetochore
spindle
• Chromosomes attach to
microtubules at the kinetochores
• Each chromosome is oriented
such that the kinetochores
of sister chromatids are
attached to microtubules
from opposite poles.
• Chromosomes move to
equator of the cell
© Andrew S. Bajer, University of Oregon
Fig. 10.11d
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
MITOSIS
Metaphase
Chromosomes
80 µm
aligned on
Kinetochore
metaphase plate microtubule
Polar microtubule
• All chromosomes are aligned
at equator of the cell, called
the metaphase plate
• Chromosomes are attached
to opposite poles and are
under tension
© Andrew S. Bajer, University of Oregon
Fig. 10.12
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
57 µm
Polar
microtubule
Centrioles
Kinetochore
microtubule
Aster
Metaphase
plate
Sister chromatids
© Andrew S. Bajer, University of Oregon
Fig. 10.11e
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MITOSIS
Anaphase
80 µm
Polar
microtubule Chromosomes
Kinetochore
microtubule
• Proteins holding centromeres of
sister chromatids are degraded,
freeing individual chromosomes
• Chromosomes are pulled to
opposite poles (anaphase A)
• Spindle poles move apart
(anaphase B)
© Andrew S. Bajer, University of Oregon
Fig. 10.13
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Metaphase
Pole
Overlapping
microtubules
Pole
Late Anaphase
Pole
Overlapping Pole
microtubules
© Dr. Jeremy Pickett-Heaps
2 µm
Fig. 10.11f
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MITOSIS
Telophase
80 µm
Nucleus reforming
Kinetochore
microtubule
Polar microtubule
• Chromosomes are clustered at
opposite poles and decondense
• Nuclear envelopes re-form around
chromosomes
• Golgi complex and ER re-form
© Andrew S. Bajer, University of Oregon
Fig. 10.11g
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
CYTOKINESIS
80 µm
Cleavage furrow
• In animal cells, cleavage furrow
forms to divide the cells
• In plant cells, cell plate forms
to divide the cells
© Andrew S. Bajer, University of Oregon
Fig. 10.11
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
INTERPHASE G2
CYTOKINESIS
MITOSIS
Prophase
Centrioles
(replicated;
animal
cells only)
Prometaphase
Metaphase
80 µm
80 µm
Chromatin
(replicated)
Mitotic spindle
beginning to form
Condensed
chromosomes
Chromosomes
aligned on
metaphase plate
80 µm
Centromere and Mitotic
kinetochore
spindle
Anaphase
80 µm
Kinetochore
microtubule
Telophase
80 µm
80 µm
80 µm
Polar
microtubule
Chromosomes
Nucleus reforming
Kinetochore
microtubule
Aster
Cleavage furrow
Nuclear
membrane
Nucleolus
Nucleus
• DN A has been replicated
• Centrioles replicate (animal cells)
• Cell prepares for division
• Chromosomes condense and
become visible
• Chromosomes appear as two
sister chromatids held together
at the centromere
• Cytoskeleton is disassembled:
spindle begins to form
• Golgi and ER are dispersed
• Nuclear envelope breaks down
• Chromosomes attach to
microtubules at the kinetochores
• Each chromosome is oriented
such that the kinetochores
of sister chromatids are
attached to microtubules
from opposite poles.
• Chromosomes move to
equator of the cell
Kinetochore
microtubule
Polar microtubule
• All chromosomes are aligned
at equator of the cell, called
the metaphase plate
• Chromosomes are attached
to opposite poles and are
under tension
© Andrew S. Bajer, University of Oregon
• Proteins holding centromeres of
sister chromatids are degraded,
freeing individual chromosomes
• Chromosomes are pulled to
opposite poles (anaphase A)
• Spindle poles move apart
(anaphase B)
Polar microtubule
• Chromosomes are clustered at
opposite poles and decondense
• Nuclear envelopes re-form around
chromosomes
• Golgi complex and ER re-form
• In animal cells, cleavage furrow
forms to divide the cells
• In plant cells, cell plate forms
to divide the cells
Fig. 10.14
Fig. 10.15
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0.7 µm
Vesicles containing
Nucleus membrane components
fusing to form cell plate
Plants
Cell wall
© B.A. Palevits & E.H. Newcomb/BPS/Tom Stack & Associates
Fig. 10.16-1
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
SCIENTIFIC THINKING
Hypothesis: There are positive regulators of mitosis.
Fig. 10.16-2
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SCIENTIFIC THINKING
Hypothesis: There are positive regulators of mitosis.
Prediction: Frog oocytes are arrested in G2 of meiosis I. They can
be induced to mature (undergo meiosis) by progesterone
treatment. If maturing oocytes contain a positive regulator of cell
division, injection of cytoplasm should induce an immature
oocyte to undergo meiosis.
Fig. 10.16-4
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
SCIENTIFIC THINKING
Hypothesis: There are positive regulators of mitosis.
Prediction: Frog oocytes are arrested in G2 of meiosis I. They can
be induced to mature (undergo meiosis) by progesterone
treatment. If maturing oocytes contain a positive regulator of cell
division, injection of cytoplasm should induce an immature
oocyte to undergo meiosis.
Test: Oocytes are induced with progesterone, then cytoplasm
from these maturing cells is injected into immature oocytes.
Remove
cytoplasm
Inject
cytoplasm
ProgesteroneArrested oocyte
Oocyte in meiosis I
treated oocyte
Result: Injected oocytes progress G2 from into meiosis I.
Fig. 10.16-5
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
SCIENTIFIC THINKING
Hypothesis: There are positive regulators of mitosis.
Prediction: Frog oocytes are arrested in G2 of meiosis I. They can
be induced to mature (undergo meiosis) by progesterone
treatment. If maturing oocytes contain a positive regulator of cell
division, injection of cytoplasm should induce an immature
oocyte to undergo meiosis.
Test: Oocytes are induced with progesterone, then cytoplasm
from these maturing cells is injected into immature oocytes.
Remove
cytoplasm
Inject
cytoplasm
ProgesteroneArrested oocyte
Oocyte in meiosis I
treated oocyte
Result: Injected oocytes progress G2 from into meiosis I.
Conclusion: The progesterone treatment causes production of a
positive regulator of maturation: Maturation Promoting Factor (MPF).
Fig. 10.16-7
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
SCIENTIFIC THINKING
Hypothesis: There are positive regulators of mitosis.
Prediction: Frog oocytes are arrested in G2 of meiosis I. They can
be induced to mature (undergo meiosis) by progesterone
treatment. If maturing oocytes contain a positive regulator of cell
division, injection of cytoplasm should induce an immature
oocyte to undergo meiosis.
Test: Oocytes are induced with progesterone, then cytoplasm
from these maturing cells is injected into immature oocytes.
Remove
Inject
cytoplasm
cytoplasm
Arrested oocyte
Oocyte in meiosis I
Progesteronetreated oocyte
Result: Injected oocytes progress G2 from into meiosis I.
Conclusion: The progesterone treatment causes production of a
positive regulator of maturation: Maturation Promoting Factor (MPF).
Prediction: If mitosis is driven by positive regulators, then
cytoplasm from a mitotic cell should cause a G1 cell to enter
mitosis.
Test: M phase cells are fused with G1 phase cells, then the
nucleus from the G1 phase cell is monitored microscopically.
M phase cell
G1 phase cell
Fused cells
Conclusion: Cytoplasm from M phase cells contains a positive
regulator that causes a cell to enter mitosis.
Fig. 10.17
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High
Concentration
MPF activity
Cyclin
Low
G2
M
G1
S
G2
M
G1
S
G2
M
Fig. 10.18
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G2/M checkpoint
Spindle checkpoint
M
G2
S
G1/S checkpoint
(Start or restriction point)
G1
Fig. 10.19
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Cyclin-dependent kinase
(Cdk)
P
Cyclin
P
Fig. 10.20
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G2/M Checkpoint
Spindle Checkpoint
Cdc2/Mitotic Cyclin
APC
• Replication
completed
• DNA integrity
• Chromosomes
attached at
metaphase plate
M
G2
G1/S Checkpoint
Cdk1/Cyclin B
S
Yeast
• Growth factors
• Nutritional state
of cell
• Size of cell
G1
Fig. 10.21
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G2/M Checkpoint
Spindle Checkpoint
Cdk1/Cyclin B
APC
• Replication
completed
• DNA integrity
• Chromosomes
attached at
metaphase plate
M
G2
G1/S Checkpoint
Cdc2/G1Cyclin
S
Animals
• Growth factors
• Nutritional state
of cell
• Size of cell
G1
Fig. 10.22
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Growth factor
P
P
P
P
P
P
P
P
Cyclins/
proteins
for S phase
P
ERK
ERK
P
RAS
RAS
Rb
Rb
MEK
E2F
Nucleus
Nucleus
RAF
Rb
Rb
P
MAP kinase pathway
Rb
P
E2F
E2F
Chromosome
Chromosome
Fig. 10.23-1
Normal p53
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p53 allows cells with
repaired DNA to divide.
p53
protein
DNA repair enzyme
1. DNA damage is caused by
heat, radiation, or chemicals.
2. Cell division stops, and p53 triggers
enzymes to repair damaged region.
3. p53 triggers the destruction of
cells damaged beyond repair.
Fig. 10.23
Normal p53
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DNA repair enzyme
1. DNA damage is caused by
heat, radiation, or chemicals.
Abnormal p53
p53 allows cells with
repaired DNA to divide.
p53
protein
Abnormal
p53 protein
1. DNA damage is caused by
heat, radiation, or chemicals.
2. Cell division stops, and p53 triggers
enzymes to repair damaged region.
3. p53 triggers the destruction of
cells damaged beyond repair.
Cancer cell
2. The p53 protein fails to stop cell
3. Damaged cells continue to divide.
division and repair DNA. Cell divides
If other damage accumulates, the
without repair to damaged DNA.
cell can turn cancerous.
Fig. 10.24
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Proto-oncogenes
Ras
protein
Src
kinase
Rb
protein
p53
protein
Cell cycle
checkpoints
Growth factor receptor:
more per cell in many
breast cancers.
Ras protein:
activated by mutations
in 20–30% of all cancers.
Src kinase:
activated by mutations
in 2–5% of all cancers.
Tumor-suppressor Genes
Rb protein:
mutated in 40% of all cancers.
p53 protein:
mutated in 50% of all cancers.

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