DOC PREVIEW
UNC-Chapel Hill BIOL 201 - Senescence

This preview shows page 1 out of 4 pages.

Save
View full document
View full document
Premium Document
Do you want full access? Go Premium and unlock all 4 pages.
Access to all documents
Download any document
Ad free experience
Premium Document
Do you want full access? Go Premium and unlock all 4 pages.
Access to all documents
Download any document
Ad free experience

Unformatted text preview:

BIOL 201 1st Edition Lecture 9Outline of Previous LectureI. Arbitrary male hypothesisa. Sensory biasb. ExampleII. Graph explanationIII. Runaway sexual selectionIV. Units of SelectionV. Selection between genesa. ExampleVI. Selection between organellesa. ExampleVII. Selection between cellsVIII. Group selectiona. ExampleIX. Species selectiona. Exampleb. Speciation and ExtinctionX. Inclusive fitnessXI. Kin selectiona. ExampleXII. Coefficient of relatednessa. EquationXIII. Hamilton’s RuleOutline of Current LectureI. Definition of SenescenceII. Evolution of Aginga. Late-acting deleterious mutationsb. Antagonistic pleiotropyc. Natural Aging ExperimentIII. Cost of sexa. Survival Costsb. Reproductive costsIV. Why sex?a. Fixation of rare beneficial mutationsb. Adaptation to variable environmentsc. Deleterious mutationsCurrent LectureI. Definition of Senescence: aging that is independent of wear and teara. Decline with age in reproductive performance, physiological function, or probability of survivalII. Evolution of Aginga. Late-acting deleterious mutationsi. Bigger deficit in fitness comes from mutations that hurt you as a child because if you die then your reproductive fitness is 0.ii. Mutations that cause death late in life are only midly deleterious because you’ve already had kids to cover reproductive fitnessiii. Natural selection against late-acting deleterious mutations is weak so their occurrence may increase due to drift and may even fix.iv. Ex: Huntingdon’s Disease and hereditary non-polyposis colon cancerb. Antagonistic pleiotropyi. Pleiotropy: when a gene has multiple effects, 2 different phenotypes from the same geneii. Is between genes that act early in life and those that act late in lifeiii. Things that happen early in life affect fitness more than things that happen later because you’re pre reproductive ageiv. Antagonistic part- advantage early in life but cost late in lifev. Selection will favorvi. Ex: genes that increase reproductive effortvii. What’s considered late in life is different depending on the species, related to life span and different accidental death ratesc. Natural Aging Experimenti. Observed island populations of Virginia Opossums compared to mainland populations; island had reduced predation ratesii. Island also have evolved lower senescence which increases their ability to reproduceiii. Population is aging more if have longer fiber breaking timeIII. Cost of sexi. Sexual reproduction has costs and a lot of organisms are asexualii. Ex: aphids; have sex sometimes and not other times so they canreproduce asexually and sexually depending on the time of yeariii. Volvoxaureus have sexual and asexual females in the population at the same timeiv. Asexual organisms are always female while males are always sexualv. Some species of whiptail lizards are sexual and others are asexualvi. Can get asexual species when two sexual organisms hybridizeb. Survival Costs: have to put effort into finding an individual of the opposite sex to mate with i. Ex: peacocksc. Reproductive costsi. Two-fold cost: asexuals in a population are increasing at twice the rate of sexuals because you need a male for every offspringIV. Why sex?i. Meiosis with crossing over and matings between unrelated individualsii. Recombination and alleles appear in different backgroundsb. Fixation of rare beneficial mutationsi. Epistasis: interaction between genes that increase fitness, superfitnessii. Clonal interference: competition between alleles at loci so only one can win evolutionarily; only occurs in asexualsiii. Images on slide 21iv. In a small population, advantageous alleles can fix quicker and drift can play a larger role; odds of clonal interference are really low; same pattern between sexual and asexualc. Adaptation to variable environmentsi. Recombination happens very quickly in sexualsii. Quicker adaptation in sexual environment than asexual oneiii. Spatial variation- advantage to sex1. Distribution to patches where competition occursa. Asexuals- all same genotype and abilityb. Sexuals- diff genotypes and abilitiesd. Deleterious mutationsi. Muller’s ratchet- graph on slide 271. Ratchet is a tool like a gear that can only go in one direction2. Mutation load: how many deleterious mutations a population carries; lots of them may send to extinction3. Lots of targets for deleterious mutations but you can’t really get rid of them as an asexual4. If have sexual reproduction, offspring could have combo of mutations or maybe none at all5. Asexual accumulate deleterious mutations much quicker than sexual ones.6. Mutational meltdown: having so many mutations that you can’t survive as a speciesii. Kondrashov’s model- variant of Muller’s ratchet1. Can have interaction btwn epistasis and Muller’s ratchet2. Maybe there’s a threshold for # of mutations and if pass it then fitness plummets3. In sexual, every generation will basically the same.4. Asexual population is constantly hanging right near the threshold ; any big change can lead to


View Full Document

UNC-Chapel Hill BIOL 201 - Senescence

Download Senescence
Our administrator received your request to download this document. We will send you the file to your email shortly.
Loading Unlocking...
Login

Join to view Senescence and access 3M+ class-specific study document.

or
We will never post anything without your permission.
Don't have an account?
Sign Up

Join to view Senescence 2 2 and access 3M+ class-specific study document.

or

By creating an account you agree to our Privacy Policy and Terms Of Use

Already a member?