Ageing and Death

Question 1

Define semelparity and iteroparity

Answer 1

Semelparity - single reproductive episode followed by death e.g. Pacific Salmon

Iteroparity - repeated reproductive episodes throughout life, before death e.g. Atlantic Salmon

Question 2

What is extrinsic and intrinsic mortality?

Answer 2

Extrinsic - death due to external factors e.g. predation, environmental extremes, starvation.

Intrinsic - death due to internal factors e.g. tissue deterioration, immuno-compromise

Question 3

Why do birds age slower than mammals?

Answer 3

Compared with equivalent-sized mammals, birds are on average 3x longer lived, despite the fact they have a higher metabolic rate.

Flight significantly lowers predation risk and extrinsic mortality.

Question 4

Why are older individuals less likely to successfully proliferate genes?

Answer 4

1) Reproduction is additive and multiplicative through time
2) Fewer individuals survive to old age

Strength of selection to survive therefore declines with age

Question 5

What is the general senescence theory?

Answer 5

Senescence occurs because the strength of selection for surviving in age-structured populations declines with age.

As you get older, the probability of dying due to extrinsic factors increases, reducing reproductive fitness.

Question 6

What are the ultimate and proximate drivers of age?

Answer 6

Ultimate - Decreasing selection on investment to remain alive as an individual ages through reproduction.

Proximate:
- Free radical damage
- Mitochondrial damage
- DNA replicative damage
- Telomere shortening

Question 7

How does mutation accumulation cause senescence?

Answer 7

Errors in genetic mechanisms through deleterious mutations e.g. cancer
Errors in physiological maintenance e.g. free radical cell damage
Deleterious alleles e.g. Huntington’s disease - single, dominant gene that disables fitness above age of 45 so selection is weak to remove it.

Question 8

How does antagonistic pleiotropy cause senescence?

Answer 8

Genes coding for investing in early life reproductive fitness antagonise with later-life survival maintenance.

Heavy investment in offspring provisioning:
- Reduces opportunity for building up fat reserves
- Increases demand to invest in extra foraging, increases predation risk
- Reduces investment available to prevent against intrinsic ageing.

Somatic maintenance sometimes shut off in semelparous taxa to maximise reproduction effort. e.g. Pacific Salmon.