1. 10 µm Fig. 12-10 Nucleus Chromatin condensing Nucleolus Chromosomes
Cell plate
Figure Mitosis in a plant cell 1
Prophase 2
Prometaphase 3
Metaphase 4
Anaphase 5
Telophase

2. Nucleus 1 Prophase Chromatin condensing Nucleolus Fig. 12-10a
Figure Mitosis in a plant cell 1
Prophase

3. Chromosomes 2 Prometaphase Fig. 12-10b
Figure Mitosis in a plant cell 2
Prometaphase

4. Fig c
Figure Mitosis in a plant cell 3
Metaphase

5. Fig d
Figure Mitosis in a plant cell 4
Anaphase

6. 10 µm Cell plate 5 Telophase Fig. 12-10e
Figure Mitosis in a plant cell 5
Telophase

7. Binary Fission
Prokaryotes (bacteria and archaea) reproduce by a type of cell division called binary fission
In binary fission, the chromosome replicates (beginning at the origin of replication), and the two daughter chromosomes actively move apart
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8. Cell wall Origin of replication Plasma membrane E. coli cell Bacterial
Fig
Cell wall
Origin of
replication
Plasma
membrane
E. coli cell
Bacterial
chromosome
Two copies
of origin
Figure Bacterial cell division by binary fission

9. Cell wall Origin of replication Plasma membrane E. coli cell Bacterial
Fig
Cell wall
Origin of
replication
Plasma
membrane
E. coli cell
Bacterial
chromosome
Two copies
of origin
Origin
Origin
Figure Bacterial cell division by binary fission

10. Cell wall Origin of replication Plasma membrane E. coli cell Bacterial
Fig
Cell wall
Origin of
replication
Plasma
membrane
E. coli cell
Bacterial
chromosome
Two copies
of origin
Origin
Origin
Figure Bacterial cell division by binary fission

11. Cell wall Origin of replication Plasma membrane E. coli cell Bacterial
Fig
Cell wall
Origin of
replication
Plasma
membrane
E. coli cell
Bacterial
chromosome
Two copies
of origin
Origin
Origin
Figure Bacterial cell division by binary fission

12. The Evolution of Mitosis
Since prokaryotes evolved before eukaryotes, mitosis probably evolved from binary fission
Certain protists exhibit types of cell division that seem intermediate between binary fission and mitosis
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13. Fig. 12-12 Bacterial chromosome (a) Bacteria Chromosomes Microtubules
Intact nuclear
envelope
(b) Dinoflagellates
Kinetochore
microtubule
Intact nuclear
envelope
Figure A hypothetical sequence for the evolution of mitosis
(c) Diatoms and yeasts
Kinetochore
microtubule
Fragments of
nuclear envelope
(d) Most eukaryotes

14. Bacterial chromosome (a) Bacteria Chromosomes Microtubules
Fig ab
Bacterial
chromosome
(a) Bacteria
Chromosomes
Microtubules
Figure A hypothetical sequence for the evolution of mitosis
Intact nuclear
envelope
(b) Dinoflagellates

15. Kinetochore microtubule Intact nuclear envelope (c) Diatoms and yeasts
Fig cd
Kinetochore
microtubule
Intact nuclear
envelope
(c) Diatoms and yeasts
Kinetochore
microtubule
Figure A hypothetical sequence for the evolution of mitosis
Fragments of
nuclear envelope
(d) Most eukaryotes

16. Concept 12.3: The eukaryotic cell cycle is regulated by a molecular control system
The frequency of cell division varies with the type of cell
These cell cycle differences result from regulation at the molecular level
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17. Evidence for Cytoplasmic Signals
The cell cycle appears to be driven by specific chemical signals present in the cytoplasm
Some evidence for this hypothesis comes from experiments in which cultured mammalian cells at different phases of the cell cycle were fused to form a single cell with two nuclei
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18. EXPERIMENT RESULTS Experiment 1 Experiment 2 S G1 M G1 S S M M
Fig
EXPERIMENT
Experiment 1
Experiment 2 S G1 M G1
RESULTS S S M M
When a cell in the
S phase was fused
with a cell in G1, the G1
nucleus immediately
entered the S
phase—DNA was
synthesized.
When a cell in the
M phase was fused with
a cell in G1, the G1
nucleus immediately
began mitosis—a
spindle formed and
chromatin condensed,
even though the
chromosome had not
been duplicated.
Figure Do molecular signals in the cytoplasm regulate the cell cycle?

19. The Cell Cycle Control System
The sequential events of the cell cycle are directed by a distinct cell cycle control system, which is similar to a clock
The cell cycle control system is regulated by both internal and external controls
The clock has specific checkpoints where the cell cycle stops until a go-ahead signal is received
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20. G1 checkpoint Control system S G1 G2 M M checkpoint G2 checkpoint
Fig
G1 checkpoint
Control
system S G1 G2 M
Figure Mechanical analogy for the cell cycle control system
M checkpoint
G2 checkpoint

21. For many cells, the G1 checkpoint seems to be the most important one
If a cell receives a go-ahead signal at the G1 checkpoint, it will usually complete the S, G2, and M phases and divide
If the cell does not receive the go-ahead signal, it will exit the cycle, switching into a nondividing state called the G0 phase
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22. (b) Cell does not receive a go-ahead signal
Fig G0
G1 checkpoint
Figure The G1 checkpoint G1 G1
Cell receives a go-ahead
signal
(b) Cell does not receive a
go-ahead signal

23. The Cell Cycle Clock: Cyclins and Cyclin-Dependent Kinases
Two types of regulatory proteins are involved in cell cycle control: cyclins and cyclin-dependent kinases (Cdks)
The activity of cyclins and Cdks fluctuates during the cell cycle
MPF (maturation-promoting factor) is a cyclin-Cdk complex that triggers a cell’s passage past the G2 checkpoint into the M phase
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

24. Protein kinase activity (– )
Fig
RESULTS 5 30 4 20 3
% of dividing cells (– )
Protein kinase activity (– ) 2 10 1
Figure How does the activity of a protein kinase essential for mitosis vary during the cell cycle?
100
200
300
400
500
Time (min)

25. M G1 S G2 M G1 S G2 M G1 Fig. 12-17 MPF activity Cyclin concentration
Time
(a) Fluctuation of MPF activity and cyclin concentration during
the cell cycle G1 S
Cdk
Figure Molecular control of the cell cycle at the G2 checkpoint
Cyclin accumulation M
Degraded
cyclin G2 G2
Cdk
Cyclin is
degraded
checkpoint
Cyclin
MPF
(b) Molecular mechanisms that help regulate the cell cycle

26. (a) Fluctuation of MPF activity and cyclin concentration during
Fig a M G1 S G2 M G1 S G2 M G1
MPF activity
Cyclin
concentration
Figure Molecular control of the cell cycle at the G2 checkpoint
Time
(a) Fluctuation of MPF activity and cyclin concentration during
the cell cycle

27. (b) Molecular mechanisms that help regulate the cell cycle
Fig b G1 S
Cdk
Cyclin accumulation M
Degraded
cyclin G2 G2
checkpoint
Cdk
Figure Molecular control of the cell cycle at the G2 checkpoint
Cyclin is
degraded
Cyclin
MPF
(b) Molecular mechanisms that help regulate the cell cycle

28. Stop and Go Signs: Internal and External Signals at the Checkpoints
An example of an internal signal is that kinetochores not attached to spindle microtubules send a molecular signal that delays anaphase
Some external signals are growth factors, proteins released by certain cells that stimulate other cells to divide
For example, platelet-derived growth factor (PDGF) stimulates the division of human fibroblast cells in culture
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29. Scalpels Petri plate Without PDGF cells fail to divide With PDGF
Fig
Scalpels
Petri
plate
Without PDGF
cells fail to divide
Figure The effect of a growth factor on cell division
With PDGF
cells prolifer-
ate
Cultured fibroblasts
10 µm

30. Another example of external signals is density-dependent inhibition, in which crowded cells stop dividing
Most animal cells also exhibit anchorage dependence, in which they must be attached to a substratum in order to divide
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31. Density-dependent inhibition
Fig
Anchorage dependence
Density-dependent inhibition
Density-dependent inhibition
Figure Density-dependent inhibition and anchorage dependence of cell division
25 µm
25 µm
(a) Normal mammalian cells
(b) Cancer cells

32. Cancer cells exhibit neither density-dependent inhibition nor anchorage dependence
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33. Loss of Cell Cycle Controls in Cancer Cells
Cancer cells do not respond normally to the body’s control mechanisms
Cancer cells may not need growth factors to grow and divide:
They may make their own growth factor
They may convey a growth factor’s signal without the presence of the growth factor
They may have an abnormal cell cycle control system
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34. A normal cell is converted to a cancerous cell by a process called transformation
Cancer cells form tumors, masses of abnormal cells within otherwise normal tissue
If abnormal cells remain at the original site, the lump is called a benign tumor
Malignant tumors invade surrounding tissues and can metastasize, exporting cancer cells to other parts of the body, where they may form secondary tumors
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35. Lymph vessel Tumor Blood vessel Cancer cell Glandular tissue
Fig
Lymph
vessel
Tumor
Blood
vessel
Cancer
cell
Glandular
tissue
Metastatic
tumor 1
A tumor grows
from a single
cancer cell. 2
Cancer cells
invade neigh-
boring tissue. 3
Cancer cells spread
to other parts of
the body. 4
Cancer cells may
survive and
establish a new
tumor in another
part of the body.
Figure The growth and metastasis of a malignant breast tumor

36. G1 S Cytokinesis Mitosis G2 MITOTIC (M) PHASE Prophase Telophase and
Fig. 12-UN1
INTERPHASE G1 S
Cytokinesis
Mitosis G2
MITOTIC (M) PHASE
Prophase
Telophase and
Cytokinesis
Prometaphase
Anaphase
Metaphase

37. Fig. 12-UN2

38. Fig. 12-UN3

39. Fig. 12-UN4

40. Fig. 12-UN5