1. Chapter 12

2. Cell Division – Why? Growth Repair Reproduction

3. The Cell Cycle Frequency of division varies by cell type

4. Interphase Longest phase (90% of cell cycle) DNA is loosely packed (chromatin) Nucleus is well-defined Three parts: G1 (Gap 1) S (Synthesis) G2 (Gap 2)

5. M Phase Two parts: Mitosis (division of nucleus) Cytokinesis (division of cytoplasm)

6. Prophase Condensation of DNA Histones Nucleosomes Chromatin Chromosomes Sister chromatids Centromere Kinetochores

7. Prometaphase Nucleus breaks down Centrioles move to poles Spindle fibers form and attach to kinetochore proteins

8. Metaphase Metaphase plate

9. Anaphase Inactivation of proteins holding chromatids together Chromatids pulled by motor proteins to opposite poles Polar spindle fibers elongate

10. Telophase Formation of daughter nuclei Spindle fibers disintegrate DNA uncoils Cytokinesis occurs simultaneously

11. Cytokinesis Animals: Actin ring forms cleavage furrow Plants: Golgi sends vesicles forming cell plate

13. Evolution of Mitosis Binary fission (prokaryotes) Intact nuclear envelope (some protists) Mitosis

14. Cell Cycle Control Two irreversible points in cell cycle Replication of genetic material Separation of chromatids Can be paused at checkpoints Chemical signals indicate cell processes are completed correctly

15. 3 Critical Checkpoints G1 (AKA “restriction point”) most critical

16. “Go-ahead Signals” Usually proteins or steroid hormones Intracellular signals: “promoting factors” External signals: “growth factors” Primary mechanism of control: phosphorylation by kinase enzymes

17. Promoting Factors Cyclin – regulatory protein Cdk’s – cyclin-dependent kinases Activate cyclin Cyclin + cdk = MPF (Mitosis Promoting Factor) APC (Anaphase Promoting Complex)

20. Growth Factors Extracellular signals that stimulate other cells to divide Density-dependent inhibition Anchorage dependence

21. Cancer p 53 & G1 checkpoint Apoptosis or repair Benign tumors Malignant tumors (metastasis)

22. Growth Factors & Cancer Proto-oncogenes Promote cell division Cancerous if mutated “on” Example: RAS (activates cyclins) Tumor suppressor genes Cancerous if mutated “off” Example: p53

23. Development of Cancer Develops only after a cell experiences ~6 key mutations Unlimited growth - turn on growth promoter genes Ignore checkpoints - turn off tumor suppressor genes Escape apoptosis - turn off suicide genes Immortality = unlimited divisions -turn on telomerase Promotes blood vessel growth - turn on blood vessel growth genes Overcome anchor & density dependence - turn off touch sensor gene

24. Kidney Cells

25. Liver Cells

26. Blood Cells

27. Colon Cells

30. Questions to Discuss What are the general defining features of normal cells? What are the general defining features of cancer cells? How does the chromosomal composition differ between normal and cancerous cells? How does the actual process of cell division differ in cancerous cells from that of normal cells? What other questions about cancer do you have?

31. Questions to Discuss Was it right to take Henrietta Lacks’s cells without permission? Why or why not? Should the family have been told sooner? Is the surviving family entitled to any compensation? If so, what? Hundreds of medical and biological advances have been made that wouldn’t have happened without HeLa cells. How does that affect your answer? If the family decided that they didn’t want HeLa cells being used any more, do you think it is within their right to demand it? Why or why not?