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The Cell Cycle. Key Concepts Most division results in genetically identical cells Cell cycle consists of alternating periods of mitosis and interphase.

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Presentation on theme: "The Cell Cycle. Key Concepts Most division results in genetically identical cells Cell cycle consists of alternating periods of mitosis and interphase."— Presentation transcript:

1 The Cell Cycle

2 Key Concepts Most division results in genetically identical cells Cell cycle consists of alternating periods of mitosis and interphase Eukaryotic cell cycle is highly regulated

3 Purpose Ultimate purpose of cell cycle is to propagate genetic information Also important for – Tissue repair – Growth – Reproduction

4

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6 Figure 12.5-1 Chromosomes Chromosomal DNA molecules Centromere Chromosome arm 1

7 Figure 12.5-2 Chromosomes Chromosomal DNA molecules Centromere Chromosome arm Chromosome duplication (including DNA replication) and condensation Sister chromatids 1 2

8 Figure 12.5-3 Chromosomes Chromosomal DNA molecules Centromere Chromosome arm Chromosome duplication (including DNA replication) and condensation Sister chromatids Separation of sister chromatids into two chromosomes 1 2 3

9 Phases of cell cycle Interphase – G1 – G2 – S Mitosis – Prophase – Metaphase – Anaphase – Telophase

10 Figure 12.6 INTERPHASE G1G1 G2G2 S (DNA synthesis) MITOTIC (M) PHASE Cytokinesis Mitosis

11 Figure 12.7 G 2 of InterphaseProphasePrometaphase Centrosomes (with centriole pairs) Chromatin (duplicated) Nucleolus Nuclear envelope Plasma membrane Early mitotic spindle Aster Centromere Chromosome, consisting of two sister chromatids Fragments of nuclear envelope Nonkinetochore microtubules Kinetochore Kinetochore microtubule Metaphase Metaphase plate AnaphaseTelophase and Cytokinesis Spindle Centrosome at one spindle pole Daughter chromosomes Cleavage furrow Nucleolus forming Nuclear envelope forming 10  m

12 Figure 12.7a G 2 of Interphase Prophase Prometaphase Centrosomes (with centriole pairs) Chromatin (duplicated) Nucleolus Nuclear envelope Plasma membrane Early mitotic spindle Aster Centromere Chromosome, consisting of two sister chromatids Fragments of nuclear envelope Nonkinetochore microtubules Kinetochore Kinetochore microtubule

13 Figure 12.7b Metaphase Metaphase plate Anaphase Telophase and Cytokinesis Spindle Centrosome at one spindle pole Daughter chromosomes Cleavage furrow Nucleolus forming Nuclear envelope forming

14 Mitotic Spindle Sister chromatids Aster Centrosome Metaphase plate (imaginary) Kineto- chores Overlapping nonkinetochore microtubules Kinetochore microtubules Microtubules Chromosomes Centrosome 0.5  m 1  m

15 Figure 12.9a Kinetochore Mark Spindle pole EXPERIMENT RESULTS

16 Figure 12.9b Chromosome movement Microtubule Motor protein Chromosome Kinetochore Tubulin subunits CONCLUSION

17 Cytokenisis

18 Figure 12.10a (a) Cleavage of an animal cell (SEM) Cleavage furrow Contractile ring of microfilaments Daughter cells 100  m

19 Figure 12.10b (b) Cell plate formation in a plant cell (TEM) Vesicles forming cell plate Wall of parent cell Cell plate New cell wall Daughter cells 1  m

20 Binary Fission Prokaryotes replicate via binary fission Genome replication starts at location called origin of replication Cell membrane pinches around midline of cell

21 Figure 12.12-1 1 Origin of replication E. coli cell Two copies of origin Cell wall Plasma membrane Bacterial chromosome Chromosome replication begins.

22 1 Origin of replication E. coli cell Two copies of origin Cell wall Plasma membrane Bacterial chromosome Origin Chromosome replication begins. Replication continues. 2 Figure 12.12-2

23 1 Origin of replication E. coli cell Two copies of origin Cell wall Plasma membrane Bacterial chromosome Origin Chromosome replication begins. Replication continues. Replication finishes. 2 3 Figure 12.12-3

24 1 Origin of replication E. coli cell Two copies of origin Cell wall Plasma membrane Bacterial chromosome Origin Chromosome replication begins. Replication continues. Replication finishes. Two daughter cells result. 2 3 4 Figure 12.12-4

25 Evolution of mitosis Eukaryotes most likely evolved from prokaryotic organisms Some organisms display intermediate “levels” of mitotic behavior.

26 Cell Cycle Regulation G 1 checkpoint G1G1 G2G2 G 2 checkpoint M checkpoint M S Control system Figure 12.15

27 Cyclins and CDKs Two types of regulatory proteins in cell cycle control: cyclins and cyclin-dependent kinases (Cdks) Cdks activity fluctuates during cell cycle because it is controled by cyclins, so named because their concentrations vary with the cell cycle MPF (maturation-promoting factor) is a cyclin- Cdk complex that triggers a cell’s passage past the G 2 checkpoint into the M phase

28 Figure 12.17a (a) Fluctuation of MPF activity and cyclin concentration during the cell cycle MPF activity Cyclin concentration Time M MM S S G1G1 G2G2 G1G1 G2G2 G1G1

29 (b) Molecular mechanisms that help regulate the cell cycle Cdk Degraded cyclin Cyclin is degraded MPF G 2 checkpoint Cdk Cyclin M S G1G1 G2G2 Figure 12.17b

30 Stop and Go Signals 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

31 Figure 12.18 A sample of human connective tissue is cut up into small pieces. Enzymes digest the extracellular matrix, resulting in a suspension of free fibroblasts. Cells are transferred to culture vessels. Scalpels Petri dish PDGF is added to half the vessels. Without PDGF With PDGF 10  m 1 2 3 4

32 External Signals A clear 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 Cancer cells exhibit neither density-dependent inhibition nor anchorage dependence

33 Cancer Normal cells undergo a transformation Typically result of genetic mutation Loss of ability to govern cell cycle – Too much growth – Not enough death Cancers typically pick up more and more mutations as they progress.


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