1. Telomeres, Mitosis, and Cancer

2. For life to exist, the information (genes) must be passed on.

3. Fig 3.5 The Cell Cycle

4. Fig 11.7 DNA replication

6. Sometimes errors are made.

7. Luckily, errors can be repaired. As they occur by DNA polymerase Error

8. Not all errors get repaired. These are mutations.

9. Telomeres are non-gene DNA at the ends of DNA strands.

10. Telomeres are shortened during DNA replication, and also by DNA damage.

11. Telomeres are non-gene DNA at the ends of DNA strands. Short telomeres will cause cells to stop replicating or cell death. The critical size is unknown.

12. Human Life Cycle high levels of telomerase very little telomerase

13. Why not produce telomerase all of the time? high levels of telomerase very little telomerase

14. Telomeres are non-gene DNA at the ends of DNA strands. Telomeres are shortened during DNA replication, and by DNA damage. Short telomeres will cause cell senescence or cell death. Telomere size is a measure of mutations.

15. Do telomere dynamics link lifestyle and lifespan? Pat Monaghan and Mark F. Haussmann TRENDS in Ecology and Evolution Vol 21 pg 47

16. Telomere length varies in different parts of adults: telomeres - mitosis stomach & blood cells....short- often

17. muscle & brain……….long- rare

18. Telomere length varies in different parts of adults: telomeres - mitosis stomach & blood cells....short- often muscle & brain……….long- rare liver & kidney……..short- rare

19. Telomere length varies in different parts of adults: telomeres - mitosis stomach & blood cells....short- often muscle & brain……….long- rare liver & kidney……..short- rare gametes……long

20. Telomeres are non-gene DNA at the ends of DNA strands. Telomeres are more sensitive DNA damage, and may act as a sensor for overall DNA damage level in a cell.

21. Does telomere length indicate longevity?

22. Zebra finch Telomere length in red blood cells of different birds Fig. 1 TRENDS in Ecology and Evolution Vol 21 pg 47 Age (years)

23. common tern Telomere length in red blood cells of different birds Fig. 1 TRENDS in Ecology and Evolution Vol 21 pg 47 Age (years)

24. albatross TRENDS in Ecology and Evolution Vol 21 pg 47 Telomere length in red blood cells of different birds

25. Leach’s storm petrel Telomere length in red blood cells of different birds Fig. 1 TRENDS in Ecology and Evolution Vol 21 pg 47

26. Zebra finch Leach’s storm petrel common tern albatross Telomere length in red blood cells of different birds, different species have different patterns of telomere length and age Fig. 1 TRENDS in Ecology and Evolution Vol 21 pg 47

27. Fig. 2 TRENDS in Ecology and Evolution Vol 21 pg 47 Telomere length in white blood cells of different aged people. Telomere length generally declines, but there is wide variability

28. THE LANCET Vol 361 pg 393 Telomere length and mortality in people over 60 years old upper 50% of telomere length lower 50% of telomere length proportion surviving % years after initial assessment

29. Telomere length may indicate biological age. Early stress may cause premature telomere degradation.

30. For life to exist, the information (genes) must be passed on. {Mitosis: producing more cells} {Meiosis: producing gametes}

31. The Cell Cycle Fig 3.5

32. Mitosis: A DNA Perspective

33. Mitosis plays a role in: Growth and Development Repair and Turnover of Cells Reproduction –Asexual

34. start of mitosis Fig 3.8

35. The Mitotic Spindle (micro- tubules) Sister Chromatids A basic look at mitosis Fig 3.7

36. Mitosis is tightly regulated: checkpoints Fig 22.16

37. Cell division is regulated by both positive and negative signals. Positive signals start the process of cell division. Negative signals inhibit cell division.

38. 2 proteins, Cyclin and Cdk, control entry into mitosis Fig 22.16

39. Cdk 2 proteins, Cyclin and Cdk, control entry into mitosis. Fig 22.16

40. Fig. 3 TRENDS in Ecology and Evolution Vol 21 pg 47 Balance between Longevity and Health

41. Mutations

42. Cancer: Cell Division Gone Wrong

43. Normal Mammalian Cells Have Contact Inhibition

44. Cancer Cells Do Not Have Contact Inhibition

45. Tumors in a Liver normal tumors

46. Cancer: is the loss of control over cell division. Tumors are normal cells that are dividing inappropriately. –They stop performing their “normal” function, and are dividing repeatedly.

47. A cell becomes cancerous when there are incorrect positive AND negative signals.

48. GO! STOP! cancer

49. Multiple mutations are required for cancer to occur Fig 22.17

50. Tbl 22.9

52. Cancer Cells Normal Cells

53. Benign versus Malignant cancer

54. How do these mutations arise?

55. Chromosome abnormalities in cancer cells Fig 22.18

56. Causes of mutations: Replication errors –Exacerbated by poor DNA repair Genetic predispositions for poor repair or already having some mutations –Limited by telomere length

57. Tbl 22.10

58. Causes of mutations: Replication errors –Exacerbated by poor DNA repair –Limited by telomere length Other biological agents –Viruses –Transposons

59. Causes of mutations: Replication errors –Exacerbated by poor DNA repair –Limited by telomere length Other biological agents –Viruses –Transposons Environmental factors –Ultraviolet light –Mutagenic chemicals smoking, industrial waste, natural toxins

60. Environment plays a large role in the chance of contracting cancer… The multiethnic cohort study: exploring genes, lifestyle and cancer risk. L Kolonel, D Altshuler, B Henderson (July 2004) Nature Reviews Cancer 4, 519-527 Fig 1