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Behavioural Ecology
Aging and death
| Question | Answer |
|---|---|
| Semelparity | A single reproductive episode followed by death |
| Iteroparity | Repeated reproductive episodes throughout life followed by death |
| Extrinsic mortality | Death due to external factors ie. predation, accidents, starvation, environmental changes |
| Intrinsic mortality | Death due to internal factors ie. physical disease/aging |
| Aging profiles of different species | Some live long, some live very little (depends on species and specific behaviours ie. honey bees - queens live 3-8 years, workers live 320 days) |
| Why do birds age slower than mammals? | Compared with equivalent-sized mammals, birds are on average 3x longer-lived Birds also have: 2 - 2.5x higher metabolic rate 15x higher lifetime metabolic expenditure 3oC higher body temperatures 2 - 4x higher blood glucose levels |
| Does flight play a role? | Bats can live 3x as long as flightless mammals, accounting for hibernation - low extrinsic mortality than terrestrial mammals? |
| Senescence (aging) | Investment is partitioned between survival and reproduction Consider a gene for promoting longevity |
| Senescence (aging) | The probability of that gene being reproduced and proliferated is dependent upon the age of the individual carrying it, (once reproduction has begun) Older individuals are less likely to successfully proliferate the gene because |
| Senescence (aging) | 1) Reproduction is additive and multiplicative through time 2) Fewer individuals survive to old age |
| Fitness relationships in a non-senescing model subject ONLY to extrinsic mortality risks | Strength of selection to survive therefore declines with age |
| General senescence theory | Senescence occurs because the strength of selection for surviving in age structured populations declines with age - as you get older, your probability of having died due to extrinsic factors increases, reducing your reproductive fitness |
| A relaxation of selection on: | 1) investment to live longer/keep alive 2) invest in later-age reproduction |
| What really makes us age? | - Ultimately intrinsic aging: DNA replicative, mitochondrial and protein damage |
| Could mutations extend lifespan? | ie. drosophila mutations can extend lifespan |
| Single gene effects on senescence | C.elegans age-1 hx546 mutant 65% increase in average lifespan 110% increase in maximum lifespan Resistance to pathological effects But reproductive output reduced under competition for resources |
| Testing aging theory | General measures of relationships between ageing - reproduction - extrinsic mortality Specific ageing theories: 1. Mutation accumulation 2a. Antagonistic pleiotropy 2b. Disposable soma |
| 1) Mutation accumulation | Maintenance of life carries inherent challenges because of: - Errors in genetic mechanisms through germ-line/spontaneous deleterious mutations - Errors in physiological maintenance - Deleterious alleles |
| Experimental evolution under increased extrinsic adult mortality rate | Drosophila replicate lines High Adult Mortality (HAM): adults killed within a few days of emergence Low Adult Mortality (LAM): adults killed after a few weeks of emergence |
| Experimental evolution under increased extrinsic adult mortality rate | Run selection lines for 5 years in this way THEN check life-history traits including adult intrinsic ageing |
| Experimental evolution under increased extrinsic adult mortality rate | After 5 years HAM lines evolved higher intrinsic mortality rate after emergence! HAM lines evolved different reproductive strategies |
| Huntington's disease | - caused by single dominant gene Why has selection not removed the gene? Because it disables fitness above age 45…. When selection to remove it is very weak |
| 2a. Antagonistic pleiotropy | Genes coding for investing in early-life reproductive fitness antagonise with later-life survival maintenance |
| 2a. Antagonistic pleiotropy | E.g. heavy investment in offspring provisioning Increases demand to invest in extra foraging, increasing predation vulnerability? Reduces investment available to prevent against intrinsic ageing |
| 2a. Antagonistic pleiotropy | Exaggeration of the mutation accumulation model due to trading investment away from maintenance and towards reproductive investment |
| Drosophila - ‘YOUNG’ and ‘OLD’ selected lines created from eggs laid on day 7 and day 25 | Artificially diverge extrinsic mortality to diverge intrinsic mortality Then controlled for reproductive effort using pupal irradiation (which stops oogenesis) |
| Drosophila | ‘Young’ selected lines had higher adult intrinsic mortality than ‘old’ selected lines (B) BUT when reproduction stopped (A), the intrinsic mortality difference between ‘old’ and ‘young’ lines disappeared |
| 2b. Disposable soma | Somatic (non-gametic) maintenance is shut-off, and resources diverted to reproduction to maximise fitness More specific and extreme form of antagonistic pleiotropy |
| Reproduction in pacific salmon - programmed senescence | - all die following reproduction = terminal investment Extreme increase in circulating levels of cortisol coincident with major primary investment in reproduction Degeneration (NOT of gonads) and death through multiple organ failure |
| Summary | Maintaining life / combating intrinsic ageing is costly Strength of selection to invest in maintenance / combat ageing declines as an individual gets older… …Because reproductive fitness declines with increasing age and cumulative extrinsic risk factors |
| Summary | Intrinsic ageing should therefore follow extrinsic mortality risks Deleterious alleles can therefore drift to fixation because of reduced selection against them later in life |
Created by:
rose.coo
Popular Ecology sets