Life History Evolution I. Components of Fitness and Trade-Offs II. Aging

1. Life History Evolution I. Components of Fitness and Trade-Offs II. Aging

2. Life History Evolution I. Components of Fitness and Trade-Offs II. Aging Fecundity and probability of survival decline later in life

3. Life History Evolution I. Components of Fitness and Trade-Offs II. Aging Fecundity and probability of survival decline later in life, so you take up golf...

4. Life History Evolution I. Components of Fitness and Trade-Offs II. Aging If senescence reduced fitness, it should be selected against. Why does aging occur?

5. Life History Evolution • I. Components of Fitness and Trade-Offs • II. Aging • A. The Rate of Living Hypothesis

6. Life History Evolution I. Components of Fitness and Trade-Offs II. Aging A. The Rate of Living Hypothesis The faster the metabolic rate, the faster the production of toxic metabolites, and the shorter the generation time. Organisms with low metabolic rates will produce less toxic waste per unit time and will have longer lives.

7. Life History Evolution • I. Components of Fitness and Trade-Offs • II. Aging • A. The Rate of Living Hypothesis • Tests • Among mammals, there is no correlation between metabolic rate and lifespan. Bats have a very high metabolic rate, but a long lifespan.

8. Life History Evolution • I. Components of Fitness and Trade-Offs • II. Aging • A. The Rate of Living Hypothesis • Tests • Selection in fruit flies revealed that you COULD select for longer lifespan. This would only support the RL model if there was also a decline in metabolic rate. there was, but only in the first 15 days, in a lifespan that lasted over 60 days.

9. Correlates between size and metabolic rate are stronger; relationships with metabolism and longevity may be a spurious artifact.

10. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis

11. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • Maybe it's not metabolic rate, but the rate of cell division.

12. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • Maybe it's not metabolic rate, but the rate of cell division. • The more divisional cycles, the more chance for a somatic mutation.

13. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • Maybe it's not metabolic rate, but the rate of cell division. • The more divisional cycles, the more chance for a somatic mutation. • Also, most cells have a prescribed number of divisions that they can perform. After this, the cell dies. Longer cell life correlates with longer organismal life

14. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis Telomeres: - Telomeres have long repeat sequences. - With each replication cycle, a short sequence is lost from the end of the chromosome (except in stem cells and cancer cells, where the enzyme telomerase reconstructs these sequences). - The shortening of telomeres correlates with aging... and organisms live longer if their cells are capable of more cell divisions.

15. 2009 Nobel Prize to Carol Greider, Jack Szostak, and Elizabeth Blackburn

16. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis Telomeres: - p53 is a tumor suppressor. - Tyner (et al. 2002): - mice who were deficient in p53 were susceptible to cancer (no repair). - They also isolated a strain that had overproduction of p53. These mutants had a reduce susceptibility to cancer, but they aged more rapidly than normal mice. - Tynan explained this as a function of the effect of p53 on stem cells. Stem cells continually produce new cells that can repair damaged tissues. If they are shut down by overproductive p53, they stop dividing. - Then, tissue damage or even simple cell death goes unrepaired or uncompensated. So, normal mice have longer life spans and intermediate levels of p53 - enough to reduce cancer rates while not shortening life too much. So, aging is the result of a balance: You need new cells, but cell divisions allow for mutations...

17. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • C. Evolutionary Theory of Aging • 1. Ideas • variation in lifespan exists and can be selected for • Why isn't it selected for in natural populations? • The Evolutionary Theory: • - aging isn't caused by the direct effects of cell and tissue damage • - rather it's the failure to repair the damage completely • - this might be caused by deleterious mutations, or trade-offs with reproduction, or selection for repair enzymes

18. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis Mutations that exert their effects early in life impose a very significant cost to reproductive success (fitness) .

19. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis Mutations that exert their effects early in life impose a very significant cost to reproductive success (fitness) However, if the expression of the same mutation can be delayed, it's effect will wane; if the effect is delayed to after reproduction the mutation is invisible to selection. .

20. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis Mutations that exert their effects early in life impose a very significant cost to reproductive success (fitness) However, if the expression of the same mutation can be delayed, it's effect will wane; if the effect is delayed to after reproduction the mutation is invisible to selection. Medewar (1952) hypothesized that aging was the cumulative effects of these delayed mutations, which cripple cell function in the end. Experiments show that one type of mutation, a mutation in repair enzymes that fix base mismatches, are only expressed post-reproductively.

21. “rat-relative DNA repair”

22. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • C. Evolutionary Theory of Aging • 1. Ideas • 2. The Mutation Accumulation Hypothesis • 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis • - If a gene exerted a positive effect on early reproduction, it would be selected for even if it also led to negative consequences later in life. • - In C. elegans, the age-1 gene has two effects. • - 1) It increases reproductive output at a young age, and • - 2) it causes senescence. Mutations in the gene increase lifespan by 80%.

23. A. The Rate of Living Hypothesis • B. Cell Division Rate Hypothesis • C. Evolutionary Theory of Aging • 1. Ideas • 2. The Mutation Accumulation Hypothesis • 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis • - If a gene exerted a positive effect on early reproduction, it would be selected for even if it also led to negative consequences later in life. • - In C. elegans, the age-1 gene has two effects. • - 1) It increases reproductive output at a young age, and • - 2) it causes senescence. Mutations in the gene increase lifespan by 80%. • Again, early reproduction really has a disproportionate affect on lifetime reproductive success. Even if a later effect is negative, even if the later effect causes DEATH, it's tough to outweigh the positive effect on fitness of early reproduction. • Once you are old, if you've reproduced, then your descendents are copying your genes faster than you could by reproducing yourself....

24. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis 4. Why such a long post-reproductive period in human females?

25. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis 4. Why such a long post-reproductive period in human females? - most animals reproduce until they die... not humans.

26. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis 4. Why such a long post-reproductive period in human females? - most animals reproduce until they die... not humans. - why, and how could this be adaptive? (think Kin Selection)

27. A. The Rate of Living Hypothesis B. Cell Division Rate Hypothesis C. Evolutionary Theory of Aging 1. Ideas 2. The Mutation Accumulation Hypothesis 3. Trade Offs - the Antagonistic Pleiotropy Hypothesis 4. Why such a long post-reproductive period in human females? - most animals reproduce until they die... not humans. - why, and how could this be adaptive? (think Kin Selection) - If a woman increases the reproductive success of her offspring (which may be numerous), she can increase her fitness more than by having one more offspring, herself.

28. Lahdenpera et al. 2004. Nature 428:178-181. - study of Finnish and Canadian women in 17-1800's, using demographic records. - women with longer life had more grandchildren. (Not producing them later, though.) Finland Canada

29. Lahdenpera et al. 2004. Nature 428:178-181. - study of Finnish and Canadian women in 17-1800's, using demographic records. - women with longer life period had more grandchildren. - the presence of a mother increased a daughters fecundity and decreased first age of rep.

30. Lahdenpera et al. 2004. Nature 428:178-181. - grandmothers increase probability of grandchildren survival. – Better if grandma isn’t too old…

31. Lahdenpera et al. 2004. Nature 428:178-181. - grandmothers increase probability of grandchildren survival. - once children stop reproducing, and grandchildren's survival is assured, the mortality rate of grandparents increases dramatically. So, in 17-1800's, the presence of grandparents increased reproductive rate of daughters and survival of grandchildren, and thus increased their own post-reproductive fitness.

32. Evo........

33. Evo........Devo

34. Evo - Devo: Evolution and Development I. Background

35. Evo - Devo I. Background - Embrologists have long realized that organisms in different phyla have different developmental "plans"

36. Evo - Devo I. Background - Embrologists have long realized that organisms in different phyla have different developmental "plans" - This is not necessarily what we might expect from random mutation and evolution... why don't we see as many differences in early developmental traits as we see in later developing traits?

37. Evo - Devo I. Background - Embrologists have long realized that organisms in different phyla have different developmental "plans" - This is not necessarily what we might expect from random mutation and evolution... why don't we see as many differences in early developmental traits as we see in later developing traits? - For instance, why do chordates have similar development, even though cartilaginous fish and other vertebrates are separated by 400 million years of divergent evolution?

38. Evo - Devo I. Background - Embrologists have long realized that organisms in different phyla have different developmental "plans" - This is not necessarily what we might expect from random mutation and evolution... why don't we see as many differences in early developmental traits as we see in later developing traits? - For instance, why do chordates have similar development, even though cartilaginous fish and other vertebrates are separated by 400 million years of divergent evolution. - Embryological development is highly conserved, while subsequently allowing extraordinary variation....

39. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED:

40. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: DNA, RNA, protein synthesis - ALL LIFE

41. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: DNA, RNA, protein synthesis - ALL LIFE Membrane structure and function - ALL EUK's

42. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: DNA, RNA, protein synthesis - ALL LIFE Membrane structure and function - ALL EUK's Cell junctions - ALL METAZOA

43. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: DNA, RNA, protein synthesis - ALL LIFE Membrane structure and function - ALL EUK's Cell junctions - ALL METAZOA Hox genes - ALL BILATERIA

44. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: DNA, RNA, protein synthesis - ALL LIFE Membrane structure and function - ALL EUK's Cell junctions - ALL METAZOA Hox genes - ALL BILATERIA Limb formation - ALL LAND VERTEBRATES

45. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: - Many enzymes are more than 50% similar in AA sequence in E. coli and H. sapiens, though separated by 2 billion years of divergence. - Of 548 metabolic enzymes in E. coli, 50% are present in ALL LIFE, and only 13% are unique to bacteria.

46. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: - Many enzymes are more than 50% similar in AA sequence in E. coli and H. sapiens. - Of 548 metabolic enzymes in E. coli, 50% are present in ALL LIFE, and only 13% are unique to bacteria. - So the variation and diversity of life is NOT due to changes in metabolic or structural genes... we are all built out of the same stuff, that works the same way at a cellular level.

47. Evo - Devo I. Background II. Core Processes - Basic biological processes are CONSERVED, and the enzymes that perform them are CONSERVED: - Many enzymes are more than 50% similar in AA sequence in E. coli and H. sapiens. - Of 548 metabolic enzymes in E. coli, 50% are present in ALL LIFE, and only 13% are unique to bacteria. - So the variation and diversity of life is NOT due to changes in metabolic or structural genes... we are all built out of the same stuff, that works the same way at a cellular level. - Variation is largely due to HOW these processes are REGULATED... 300 cell types in humans, all descended from the zygote; all genetically the same.

48. Evo - Devo I. Background II. Core Processes III. Weak Linkage Regulation - Development is NOT a single process

49. Evo - Devo I. Background II. Core Processes III. Weak Linkage Regulation - Development is NOT a single process - Development is a well choreographed dance of many parallel processes...

50. Evo - Devo I. Background II. Core Processes III. Weak Linkage Regulation - Development is NOT a single process - Development is a well choreographed dance of many parallel processes... - How is the parallelism maintained, ESPECIALLY as one process evolves?