2. “ALL CELLS COME FROM PRE- EXISTING CELLS”

3. Cell Division What are two different types of reproduction? WHAT MUST TAKE PLACE FOR A CELL OR ORGANISM TO REPRODUCE?

4. Bacterial cell division (binary fission)

5. Eukaryotic Cell Division (Mitosis) is much more complex What are some of the roles of mitosis in eukaryotes?

6. The functions of Mitotic cell division: 1.) Reproduction Asexual reproduction of a unicellular, eukaryotic organism

7. 2.) Development

8. 3.) Tissue renewal in adults

9. Figure 12.2 Eukaryotic chomosomes

10. Figure 12.3 Chromosome duplication and distribution during mitosis

11. Figure 12.0 Mitosis

12. Figure 12.4 The cell cycle

13. Figure 12.5 The stages of mitotic cell division in an animal cell: G 2 phase; prophase; prometaphase

14. Figure 12.5 The stages of mitotic cell division in an animal cell: metaphase; anaphase; telophase and cytokinesis. Pig cell mitosis

16. Figure 12.8 Cytokinesis in animal and plant cells

17. “To divide or not to divide, that is the question”

18. Anchorage Dependence and Density-dependent inhibition of cell division

19. External Signaling: G 1 checkpoint, Growth factors Ex. PDGF receptor cell cycle control

20. BIOLOGY OF CANCER Cancer is the loss of normal cell cycle regulation (a cell starts dividing out of control) What can cause this? Genes that play a role in normal cell cycle control are altered in some way. 1. Genes that stimulate cell division Normal version of gene: Proto-oncogene Mutated version: Oncogene

21. Mechanical analogy for the cell cycle control system

23. 2. Tumor Suppressor Genes: Two Classes - Genes involved in blocking cell division (checkpoints) - DNA Repair Genes (fix mutations in DNA) Most common examples: Rb, retinoblastoma. Involved in childhood cancer (two defective copies are required for disease ), but also in adult tumors such as bladder, breast and lung carcinoma. The Rb protein is a key target for the oncogene products of many tumor viruses, including SV40, adenoviruses, and papillomaviruses. They all bind to Rb and inhibit its activity. P53 is mutated in 50% of all cancers. It’s a target of the same tumor viruses That target Rb. P53 is required for apoptosis induced by DNA damage APC: is mutated in hereditary colon cancer BRCA1 and 2: responsible for hereditary breast cancer

24. To develop cancer it takes multiple mutations in the same cell. At least two mutations: One oncogene, one tumor suppressor gene. Some people are predisposed to getting a particular type of cancer. (Genetic Pre-dispositions)

26. The growth and metastasis of a malignant breast tumor Terminology: Tumor (benign and malignant) Metastasis

27. So what causes these mutations that can result in the development of Cancer??? Environmental Exposure: -Radiation -Viruses -Air (indoor and outdoor) and water pollution -Consumer products -Food -Cosmetics -Medicines -TIME!

28. How do we cure cancer? Prevention Treatment old and new drugs Examples: endostatin and angiostatin retinoic acid to induce differentiation inhibitors of farnesylation (Ras oncogene) Herceptin (antibodies against erbB-2 gene) Inhibitor of specific protein tyrosine-kinases (Gleevec)

30. “ASEXUAL OR SEXUAL, THAT IS THE QUESTION” REPRODUCTION

31. Figure 13.1 The asexual reproduction of a hydra

32. Figure 13.2 Two families

33. The human life cycle

34. Three sexual life cycles differing in the timing of meiosis and fertilization (syngamy) Alternation of generations

35. Human female chromosomes shown by bright field G-banding

36. Homologous pair Haploid chromosome # = n (humans: n =23) Diploid # =2n (humans: 2n = 46) Eggs & sperm All other cells (somatic)

38. The human life cycle

39. Overview of meiosis: how meiosis reduces chromosome number

40. The stages of meiotic cell division: Meiosis I

41. The stages of meiotic cell division: Meiosis II

42. A comparison of mitosis and meiosis

43. Figure 13.9 The results of alternative arrangements of two homologous chromosome pairs on the metaphase plate in meiosis I (Independent Assortment)

44. For 2 homologous chromosomes: 4 possible gametes (2 2 ) For 23 homologous chromosomes: 2 23 = 8 million possible gametes! So, upon formation of a zygote, 8 mil. X 8 mil. = 64 trillion!

45. Figure 13.10 The results of crossing over during meiosis

46. Sources of genetic variability: 1.Independent assortment 2.Crossing over (recombination) 3.Random fertilization of ovum by sperm. 4.MUTATION - ultimate source of genetic variability

47. ERRORS IN MEIOSIS

49. Testing a fetus for genetic disorders

50. The risk of nondisjunction increases dramatically with age. 30 yr. old mother: 1/1000, 40 yr. old mother: 1/100

52. GAMETOGENESIS Spermatogenesis- 48 days

53. Oogenesis- 12-50 years