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Transcript
Chapter 12
The Cell Cycle
PowerPoint® Lecture Presentations for
Biology
Eighth Edition
Neil Campbell and Jane Reece
Lectures by Chris Romero, updated by Erin Barley with contributions from Joan Sharp
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Overview: The Key Roles of Cell Division
• The continuity of life is based on the reproduction of
cells, or cell division
• In unicellular organisms, division of one cell reproduces
the entire organism
• Multicellular organisms depend on cell division for:
– Development from a fertilized cell
– Growth
– Repair
• Cell division is an integral part of the cell cycle, the
life of a cell from formation to its own division
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Concept 12.1: Cell division results in genetically
identical daughter cells
• Mitosis = Most cell division results in somatic cells
(nonreproductive cells) - two sets of chromosomes with identical
genetic information, DNA
• Meiosis = A special type of division produces nonidentical
daughter cells (gametes; reproductive cells; sperm and egg cells)
and have half as many chromosomes as somatic cells
• Genome - all the DNA in a cell
–
can consist of a single DNA molecule (common in prokaryotic
cells)
–
number of DNA molecules (common in eukaryotic cells)
• DNA molecules in a cell are packaged into chromosomes
• Eukaryotic chromosomes consist of chromatin, a complex of DNA
and protein that condenses during cell division
Fig. 12-4
0.5 µm
Chromosomes
Chromosome arm
DNA molecules
Chromosome
duplication
(including DNA
synthesis)
Centromere
Sister
chromatids
Separation of
sister chromatids
Centromere
Sister chromatids
Phases of the Cell Cycle
• The cell cycle consists of
– Mitotic (M) phase – mitosis (division of the
nucleus) and cytokinesis (division of the cytoplasm)
– Interphase (cell growth and copying of
chromosomes in preparation for cell division)
• Interphase (about 90% of the cell cycle) can be divided
into subphases:
– G1 phase (“first gap”)
– S phase (“synthesis”)
– G2 phase (“second gap”)
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 12-5
G1
S
(DNA synthesis)
G2
Fig. 12-6
G2 of Interphase
Centrosomes
Chromatin
(with centriole (duplicated)
pairs)
Prophase
Early mitotic Aster Centromere
spindle
Nucleolus Nuclear Plasma
envelope membrane
Chromosome, consisting
of two sister chromatids
Metaphase
Prometaphase
Fragments Nonkinetochore
of nuclear
microtubules
envelope
Kinetochore
Kinetochore
microtubule
Anaphase
Cleavage
furrow
Metaphase
plate
Spindle
Centrosome at
one spindle pole
Telophase and Cytokinesis
Daughter
chromosomes
Nuclear
envelope
forming
Nucleolus
forming
•Mitotic spindle - (apparatus of
microtubules that controls
Sister
chromosome movement) include: chromatids
Aster
Centrosome
Metaphase
plate
•Centrosome - microtubule
organizing center
•spindle microtubules
•Asters - radial array of short
microtubules that extends from
each centrosome
•Kinetochores - some spindle
microtubules attach to
chromosomes and move them
Kinetochores
Overlapping
nonkinetochore
microtubules
Kinetochore
microtubules
•Nonkinetochores push against each
other elongating the cell
•Metaphase plate - midway point
between the spindle’s two poles
0.5 µm
•In animal cells, cytokinesis occurs by a process known as
cleavage, forming a cleavage furrow. In plant cells, a cell plate
forms during cytokinesis
100 µm
Cleavage furrow
Contractile ring of
microfilaments
Vesicles
forming
cell plate
Wall of
parent cell
Cell plate
1 µm
New cell wall
Daughter cells
(a) Cleavage of an animal cell (SEM)
Daughter cells
(b) Cell plate formation in a plant cell (TEM)
Fig. 12-11-4
•Prokaryotes
(bacteria and
archaea)
reproduce by cell
division called
binary fission
•Chromosomes
replicate
(beginning at the
origin of
replication), and
the two daughter
chromosomes
move apart
Cell wall
Origin of
replication
E. coli cell
Two copies
of origin
Origin
Plasma
membrane
Bacterial
chromosome
Origin
Fig. 12-12
Bacterial
chromosome
(a) Bacteria
Chromosomes
Microtubules
The
Evolution
of
Intact nuclear
envelope
(b) Dinoflagellates
Kinetochore
microtubule
Mitosis
Intact nuclear
envelope
(c) Diatoms and yeasts
Kinetochore
microtubule
Fragments of
nuclear envelope
(d) Most eukaryotes
•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
Fig. 12-14
Cell cycle control
system is similar to
a clock regulated by
both internal and
external controls
G1 checkpoint
Control
system
G1
M
M checkpoint
G2
G2 checkpoint
S
Fig. 12-15
G0
G1 checkpoint
G1
G1
(a) Cell receives a go-ahead
signal
(b) Cell does not receive a
go-ahead signal
•G0 phase - a nondividing state
The Cell Cycle Clock: Cyclins & Cyclin-Dependent Kinase
• Two types of regulatory proteins are involved in
cell cycle control: cyclins and cyclindependent kinases (Cdks)
• The activity of cyclins and Cdks fluctuates
during the cell cycle
• MPF (maturation-promoting factor) is a cyclinCdk 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
Fig. 12-17
M
S
G1
G2
M
G1
S
G2
M
G1
MPF activity
Cyclin
concentration
Time
(a) Fluctuation of MPF activity and cyclin concentration during
the cell cycle
Degraded
cyclin
G2
checkpoint
Cyclin is
degraded
MPF
Cdk
Cyclin
(b) Molecular mechanisms that help regulate the cell cycle
Cyclin accumulation
Cdk
Stop and Go Signs: Internal and External Signals at
the Checkpoints
• Internal signal examples
–
kinetochores not attached to spindle
microtubules send a 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
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 12-18
Scalpels
Petri
plate
Without PDGF
cells fail to divide
With PDGF
cells proliferate
Cultured fibroblasts
10 µm
Fig. 12-19
•Density-dependent
inhibition - crowded
cells stop dividing
Anchorage dependence
Density-dependent inhibition
Density-dependent inhibition
•Anchorage
dependence (found in
most animals) - must
be attached to a
substratum in order to
divide
25 µm
25 µm
(a) Normal mammalian cells
(b) Cancer cells
Loss of Cell Cycle Controls in Cancer Cells
• Cancer cells exhibit neither density- dependent
inhibition nor anchorage dependence
• 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
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
• 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
– at the original site = benign tumor
– Malignant tumors = invade surrounding
tissues
• Metastasize, exporting cancer cells to other
parts of the body, where they may form
secondary tumors
Copyright © 2008 Pearson Education, Inc., publishing as Pearson Benjamin Cummings
Fig. 12-20
Lymph
vessel
Tumor
Blood
vessel
Cancer
cell
Metastatic
tumor
Glandular
tissue
1 A tumor grows
from a single
cancer cell.
2 Cancer cells
invade neighboring 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.