Download Why do cells reproduce?

Outline – Cell Reproduction
How Cells Divide
Why do cells divide?
Cell reproduction in prokaryotes
Cell cycle
Chromosome structure
Cell Division: Mitosis & Cytokinesis
Cancer & Cell Division
Fig. 11.2
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Binary Fission in Prokaryotes
1. Replication of DNA
Why do cells reproduce?
Prokaryote Cell
1. Single celled organisms – reproduction of species
2. Cell Growth
2. Multicellular organisms
3. FtsZ Protein ring forms
1. Growth – increase number of cells
4. Septum Forms
2. Maintenance of existing cells
3. Repair of damaged cells
5. Daughter cells form
Daughter Cells
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3
1
Fig. 11.5
Cell Division in Prokaryotes
Chromosome Structure
1. Genetic information = single, circular DNA
2. Prokaryotic cell division = binary fission
3. DNA replication is first.
4. Protein ring forms.
5. Septum (cross wall) forms.
6. One genome goes to each daughter cell
Fig. 06.05
Karyotype
Genome Size Varies
and
Homologous
Chromosomes
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Fig. 11.6
Chromosome Structure
4. Scaffold
protein
Chromosome Structure and Replication
5. Chromatin loop
30
nm
DNA
Histone
3. Solenoid
2. Nucleosome
(200 nucleotides)
6. Chromatin loops
1. DNA
7. Chromosome
1.4 X106 nucleotides
per chromosome
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Cell Cycle
Cell Cycle
M
Mitosis (M)
Metaphase
Prophase
Cytokinesis (C)
Anaphase
Telophase
C
C
G2
G2
Interphase = G1 S G2
S
Interphase (G1, S, G2 phases)
Mitosis (M)
G0
G1
S
Cytokinesis (C)
Go
G1
3
Cell Cycle
Mitosis in Eukaryotes
• Interphase
– G1 – primary growth phase
– S – DNA synthesis – Genome replication
– G2 – Preparation for mitosis
– Chromosomes condense
– Organelles replicate
Stages of Mitosis
Prophase
Metaphase
• Reproductive Phase
Anaphase
– M – Mitosis - Separation of Chromosomes
– C – Cytokinesis – Cytoplasm divides
• G0 – Resting or expression of cell fate.
Fig. 11.12b(TE Art)
Mitosis – Separation of chromosomes
“Division” of nucleus
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Interphase (at G2)
Telophase
Cytokinesis – Separation of cytoplasm
Fig. 11.12f(TE Art)
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Kinetochore
MITOSIS
Prophase
Nucleus
Centrioles
Chromosomes
condensing
Nuclear membrane
Chromatin (replicated)
Aster
1. DNA has replicated
2. Centrioles replicate
Mitotic spindle beginning to form
Centromere and kinetochore
•Nuclear membrane disintegrates
•Nucleolus disappears
•Chromosomes condense
•Mitotic spindle begins to form and is complete at end of prophase
•Kinetochores form at centromeres and attach to spindle
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Fig. 11.11(TE Art)
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Metaphase Chromosome
MITOSIS Metaphase
Centrioles
Chromosome
Aster
Microtubules
Aster
Metaphase
plate
Spindle fibers
Cohesin
proteins
Chromatid
Centromere
region of
chromosome
Kinetochore
Microtubules
Polar
Microtubules
Aster
Microtubules
Kinetochore
Kinetochore
microtubules
Sister
Chromatids
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Fig. 11.12o(TE Art)
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MITOSIS
Anaphase
Fig. 11.12p(TE Art)
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MITOSIS
Telophase
Chromosomes
Polar
Microtubules
of Spindle
Apparatus
Polar microtubules
elongate
Kinetochore
microtubules
get shorter
•Polar microtubules continue to elongate
•Chromosomes reach poles of cell
•Kinetochores disappear
•Nuclear membrane re-forms
•Nucleolus reappears
•Chromosomes decondense
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Fig. 11.12n(TE Art)
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Mitosis in Plant Cells
Cytokinesis
Cell plate in plant cells
Cell plate
Animal Cells form a
Cleavage furrow
Plant cells: cell plate forms
Animal cells: cleavage furrow forms
Interfering with Cell Division
Cancer therapies:
Controlling the Cell Cycle
Radiation & Chemotherapy
Periwinkle - Vinblastin
Pacific Yew - Taxol
Copyright © 2005 Pearson Education, Inc. Publishing as Benjamin Cummings
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Fig. 11.16(TE Art)
G2 / M checkpoint
Control of Cell Cycle
Spindle checkpoint
M
Inhibitory
phosphate
C
G2
2. Attachment of activating
phosphates by CdK
Control of the Cell Cycle
S
1. Attachment of cyclins to
activate cyclin dependent kinase
(CdK)
G1
3. Removal of inhibitory
phosphates by phosphatase
Activating
phosphate
G1 / S checkpoint
(START or Restriction Point)
Fig. 10.20
Fig. 10.22
Signal transduction pathway
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Key Proteins in
Human Cancers
PROTO-ONCOGENES
Growth factor receptor:
more per cell in many
breast cancers.
Ras
Signal
protein
transduction
pathway
Src
kinase
Cytoplasm
Rb
protein
Tumors
Ras protein:
activated by mutations
in 20–30% of all cancers.
Src kinase:
Tumor
activated by mutations
in 2–5% of all cancers.
Lymph
vessels
Blood
vessel
TUMOR-SUPPRESSOR GENES
Nucleus
p53
protein
Cyclins
Cyclin-Dependent Kinases
Phosphatases
Rb protein:
mutated in 40% of all
cancers.
p53 protein:
Continue Past
Cell cycle
checkpoints
mutated in 50% of all
cancers.
Single
cancer
cell
Invade
Neighboring
Tissue
Metastasize
END Mitosis
END
Mitosis
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