Study guide- final PDF

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final exam study guide for population evolution
with Dr. Summers...

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1) Where are the oldest hominin fossils found? - Africa 2) How are apes, hominins, old world monkeys and new world monkeys related? – they share a common ancestor from 66 million years ago (Cattarhini clade) 3) In what order did the distinctly human traits evolve over the course of evolutionary history? 4) How are the Neanderthals related to other hominids? – common ancestor, dna, physical features like appearance, speech capability, physiology 5) Based on patterns of colonization, which human population should have the highest genetic diversity? – southern Europe 6) Compare and contrast the multiregional model to the out-of-Africa model of human evolution. Multiregional model- hominins across Old World were a single species connected by gene flow - differences the result of local adaptation Out-of-Africa- all human populations are derived from recent African ancestry 7) What traits characterized the genus Australopithecus? – small brain size, high cheekbones, molar cusps, small body size, long upper limbs, heel bone 8) Where, outside of Georgia are alleles of the Denisovians found? – Kvemo kartli region 9) When did modern humans leave Africa? – 60,000 years ago 10) Why do human populations outside of Africa show generally lower genetic diversity? 11) What is the evidence that social interactions favored the evolution of large brain size in the hominid lineage? - brain size increased as they evolved (sociality is associated w/ intelligence); 12) What do we know about the evolution of language in hominids? – FOXP2 gene- specific effects on lang abilities (affects lang center in brain) (under strong pos selection in human lineage) 13) What selection pressures likely favored bipedality in the hominid lineage? 14) What was the pattern of environmental change during hominin evolution in Africa? – emergence of savannas and woodlands/grasslands 15) Did Neanderthals interbreed with Homo sapiens? - yes 16) How do Alpheus shrimp in Panama illustrate the process of allopatric speciation? – Isthmus of panama created geographic separation  separated gene pools diverge through diff mechanisms (natural selection, genetic drift, gene flow)  diff mutations arise, natural selection acts on sep organisms, gen drift alters allele freq  reproductive isolation may arise as by-product of selection or drift  populations diverge genetically 17) Why doesn’t the biological species concept apply to bacteria? Bacteria usually reproduce asexually, and even when they do sexually reproduce, they do not exchange genes the way that most prok do

18) Why is allopatric speciation more common than sympatric speciation? – geographic isolation greatly reducing gene flow btwn populations is more common (sym = ongoing gene flow) 19) How has speciation occurred in Galapagos finches? – finches are isolated on island; each species of finch developed a unique beak to adapt. The birds don’t breed with one another and have developed into unique species w/ unique characteristics (allopatric speciation) 20) What are the key differences the have led to reproductive isolation between the monkeyflower species discussed in the text? – both species are closely related but attract different pollinators (one attracts bees and the other hummingbirds) flower that attracts bees are short and have big petals for bee to land/stand on; flower for hummingbirds are long and narrow. Also each is faithfully attracted to a certain color so flowers are color in accordance to pollinator 21) Describe the differences between the biological, ecological and phylogenetic species concepts. – biological ability to interbreed and produce viable offspring is key Ecological  effect of natural selection is key Phylogenetic  identification of monophyletic groups of populations is key 22) Arrange the terms Species, Kingdom, Genus, Phylum, Class, Family and Order from least to most specific. – kingdom  phylum  class  order  family  genus  species 23) Why are mules not considered to be a separate species? – offspring of donkey and horse; sterile so cannot reproduce. Species is a group of organisms that can interbreed and create viable offspring 24) Describe problems with the biological species concept. Only applicable to the present Doesn’t apply to asexual organisms What about hybrids? 25) How are separate species designated under the phylogenetic species concept? – as monophyletic groups 26) Describe the basic forces underlying the biological, ecological and phylogenetic species concepts, and discuss how they interact. 27) How did Jason Bond designate species in Promyrmekiaphila spiders? Studied spider’s evolutionary history and ecological role (gene flow & ecological niche); sequenced the genes using all info to group into six species 28) What are the main prezygotic and postzygotic isolating mechanisms? Prezygotic – traits that prevent fertilization (habitat choice, temporal isolation, mate choice, mechanical isolation) Postzygotic – low fitness of hybrid offspring (hybrid unviability, hybrid sterility, low fitness of F2 hybrids)

29) What are the main modes of speciation? – allopatric, parapatric, and sympatric speciation 30) Compare and contrast allopatric, parapatric and sympatric speciation. Describe an example of each. Allo – geographically isolated populations (ex. Alpheus shrimp in Panama) Para- continuously distributed population; geographic barrier emerges that only partially isolates two populations/ gene flow reduced not eliminated (ex. Distribution of carrion & hooded crows in Europe) Sym- within range of the ancestral pop; not geographically separated from each other & can exchange migrants. New alleles accumulate indep. b/c indiv rarely interbreed (ex. Two populations of Rhagoletis flies; one pop lives only on hawthorn trees, the other on apple trees. They emerge as adults in spring after pupating @ diff times & the two diff trees blossom @ diff times of year) 31) What is the evidence for sympatric speciation in Rhagoletis flies? -see example above 32) What species was Homo floresiensis most closely related to? Homo erectus 33) What is “Evolutionary Medicine”? – integrated study of evolution and medicine to improve scientific understanding of the reasons for disease and actions that can be taken to improve health 34) Why do most medical school curricula not include much evolutionary biology? – lack of curriculum time, lack of faculty expertise, lack of funding, etc 35) Why has natural selection left the body so vulnerable to disease? Describe six reasons why disease exists. – disease is not shaped by selection but vulnerability to disease is 1. mismatch: body in a novel environment (coevolution: pathogens evolve faster than hosts) 2. competition w/ fast evolving organisms (natural selection lags behind environmental change) 3. every trait is a trade-off (tradeoffs make it nearly impossible for nat. selection to solve certain biological probs) 4. constraints on natural selection (a species’ evolutionary history puts constraints on potential changes nat. selection can bring out) 5. organisms shaped for R/S not health (some traits increase reproductive fitness at the cost of increasing vulnerability to disease) 6. defenses and suffering (what may appear to be a disease may actually be an adaptation) 36) Describe how recent changes over the course of human evolution have led to mismatches between our bodies, minds and environment. – our bodies were never designed to cope w/ this novel environ, selection is slow, mismatch explains most chronic disease, our fulfilled desires are killing us 37) What recent changes have occurred in the human diet due to the development of agriculture, urbanization and the industrial and technological revolutions? Compare our diets to those of huntergatherers. - human ancestors lived as hunter-gatherers but conditions ended thousands of years ago; we haven’t had time to evolve a physiological response to the superabundance created by the

extremely rapid changes in culture & technology that have occurred recently (influx of refined carbs & trans-fat in our diets, less exercise) Paleolithic – consumed more lean meat/whole foods, more exercise Modern – omega-6, sat/trans fats, refined carbs, meat from animals fed same thing, little exercise 38) What did Strassman’s study of the Dogon indicate? How is the use of birth control in modern societies related to the prevalence of breast cancer? – women of modern societies start menstruation earlier and have more menstrual cycles during lifetime than traditional societies; large scale tissue replacement in reproductive organs, enhanced levels of cell division  increased opportunity for mutations 39) Why are humans especially vulnerable to choking? How does this relate to our evolutionary history? – human throat, trachea, and esophagus evolved from aquatic ancestry; since we’ve evolved for speech production, the larynx is positioned lower and since air comes through mouth it leaves tracheal opening exposed (epiglottis only partially covers) 40) Why can't we develop antibiotics that permanently prevent bacterial infections? – bacterial antigens mimic our proteins and develop resistance against antibiotics 41) How does the disease hemochromatosis illustrate the importance of tradeoffs when thinking about the evolution of human disease? – hemochromatosis: genetic disorder that causes iron overloading – too much iron absorbed from food – can be fatal. Disorder takes iron from macrophages  low iron levels in macrophages makes them resistant to deadly infections 42) Why are most organ systems (e.g. the human eye) imperfect? – blind spot in eye, 43) How does the vulnerability of humans to choking on food illustrate the roll of evolutionary constraints on human health? 44) How can we distinguish between symptoms that are part of defenses versus those that are harmful defects or damage? – defenses: pain, fever, cough, nausea, anxiety, etc. (we can usually block them safely!) defects: seizures, cancer, paralysis, jaundice, injury 45) Describe a case in which uncomfortable symptoms of a disease are actually beneficial to the host. Having a cold: cough, fever, runny nose but they’re actually defense mechanisms 46) What is the "Smoke Detector Principle"? How does it relate to the general practice of medicine? – monitor cues associated w/ danger; if the cost of the defense is less than the expected reduction in harm from the danger then it is worth expressing the defense. Optimal regulation system expresses many normal false alarms, this is why we can block defenses safely 47) Give a proximate and ultimate definition of senescence. – a ‘progressive, generalized impairment of function, resulting in an increasing probability of death’; evolutionary definition (a ‘decline in future fitness affected by reductions in fertility as well as survival’) 48) What is the evidence that senescence occurs?

49) Describe patterns of senescence of different species in their natural environments. – chimpanzees have the same senescence pattern as humans but their life expectancy is half (in years); daphnia, drosophila mortality rate dramatically increases after a certain number of days 50) Why is the wear and tear hypothesis of senescence inconsistent with the evidence? – germ line cell lineages are immortal, some species don’t show sen., there is genetic variation in sen. within populations, there is a dramatic variation in sen. btwn species, organisms develop from single cell 51) Describe the mutation accumulation and antagonistic pleiotropy hypotheses for the evolution of senescence. Mutation accumulation theory: recurrent, deleterious mutations occur, fewer bearers survive to express later-acting mutations, the force of natural selection against them therefore declines w/age, these mutations can therefore reach a higher freq under mutation-selection balance Pleiotropy (trade-off) theory: suppose that mutations are beneficial in youth, but @ price of higher rate of ageing, more indiv will survive to express the early benefit than will live to suffer the higher rate of ageing, mutations like this can be incorp. by nat. selection 52) Explain the difference between the mutation accumulation and the antagonistic pleiotropy hypothesis for the evolution of senescence. See above 53) Why are bats especially long-lived compared to other mammals of similar size? – genes for two proteins are involved in growth – GHR and IGF1R are linked w/ longevity. These genetic changes are also responsible for dwarfism (size of bats) 54) What is the effect of extrinsic mortality on senescence? Describe the results of the Stearns et al. 2000 experiment with Drosophila. Tradeoff btwn reproduction & survival. Early fecundity 55) How did Partridge et al. 1999 demonstrate that mortality rates are associated with reproductive effort in Drosophila ? - Overlapping generations; longevity increased to 46.8 days in “old” lines, relative to a mean of 35.7 days in the base and “young” controls but old lines showed a decrease in fertility of 30-40% 56) What evidence is there for a tradeoff between reproductive effort early in life and survival later in life? - **trade-off btwn energy allocated to reproduction & its effect on future fecundity/survival (ex. Amphibians – lay large clutches of eggs but low mortality rate) 57) Describe a gene that has antagonistically pleiotropic effects. – hx546 allele; increases the reproductive success of its carriers in young adulthood, at the cost of a shorter lifespan 58) In what way(s) is cancer an evolutionary process? – tumors evolve by mutation and selection acting on cells in a tissue (multistage carcinogenesis: tumor genesis  metastasis) 59) Why is the study of cancer important in evolutionary biology? How is it relevant to other aspects of evolution? 60) What is Peto’s Paradox? – the lack of correlation btwn body mass and cancer risk (ex. Whales and elephants)

61) How did Tyner et al 2002 demonstrate a tradeoff between senescence and cancer? – selective tradeoffs inherent in mechanisms that limit the occurrence and growth of cancer cell lineages in terms of reduced capacity for repair and regeneration 62) What is the role of p53 in tradeoffs between senescence and cancer? – p53: a major gene involved in regulation of cell growth and replication. P53 surveillance prevents stem cells from replicating in the process of tissue repair – enhances rate of senescence 63) What is the difference between Caretaker and Gatekeeper genes? – caretakers: longevity assurance (dna repair), gatekeepers: tumor-suppression genes (cell death or cell cycle arrest). Increased activity of caretaker  decrease cancer and increase longevity; increased act. of gatekeepers  decrease cancer and longevity 64) What evidence is there for tradeoffs between senescence and cancer in humans? Is there any evidence against such tradeoffs? – p53 gene; significant neg correlations w/ various diseases (ex. Higher levels of apoptosis will increase # of dead neurons  greater stroke severity, but stronger apoptosis signal reduces risk of cancer) 65) Why are individuals in populations under strong selection subject to higher risk of cancer? – disrupts finely-tuned developmental programs  increases the risk that cell lineages will escape from the normal mechanisms of control of cell growth & replication, and hence become cancer cell lineages 66) Why are tissues under strong selection for rapid growth particularly vulnerable to cancer? 67) Why are elephants particularly resistant to cancer? – they have extra copies of a tumor-suppressing gene (p53); humans have only one copy, but elephants have 20 68) What parallels are there between the development of cancer within an individual and natural selection in a population? 69) How can evolutionary biology help develop treatments for cancer? – roles of selection/genetic drift in the origin of cancerous cell lineages, amplification of cancer risk via mutations relatively early in development, hypermutability of cancer cells which generates a tremendous range of variation, interplay of cancer cell pop size & mutational dynamics, ecological adaptation of cancer cells to particular cellular niches, & ‘tumor-escape’ phenotypes (just know like 3) 70) What is causing the sixth mass extinction event? – changes to the climate and landscape of the world, growing human population, and increasing demand for resources 71) Why is there a conflict between environmentalists and economists over consumption? – environmentalists: crucial to reduce consumption to avoid environmental catastrophe; economists: increasing consumption is desirable 72) Why is the term “Noble Savage” misleading? – their lower ecological impact was a function of lower population densities and less powerful technologies; they are actually not ideal conservationists 73) What caused the demographic transition? – reproductive success associated w/ wealth within traditional societies (curbing reproduction when child survival is high to help population)

74) What is the tradeoff hypothesis for the evolution of virulence? – trade-ff btwn how long a pathogen persists in its host and the rate at which it is transmitted; suggests that virulence will evolve to a level at which virulence and transmission are balanced so as to maximize the spread of the pathogen 75) What factors select for increased virulence of pathogens? – 1) coincidental evolution, 2) shortsighted evolution, 3) trade-off hypothesis 76) How is the virulence of a parasite influenced by it’s opportunities for transmission to new hosts? – selection within host favors rapid replication (increased virulence); selection across hosts favors reduced virulence 77) Why are parasites that are transported from host to host by vectors particularly virulent? – these parasites rely on host to become more vulnerable when contracting virus (ex. Malaria) when someone contracts malaria, they become so sick they “stay in bed” making them vulnerable to more mosquitos w/ more parasites (then parasite evolves further inside host through mutation & nat selection); compared to ex. flu virus that relies on host to transfer to other hosts (through sneezing/coughing so if host stays away from others than parasite can’t move on to other host)

78) How did John Snow demonstrate that cholera is a water-borne disease? – created geographic analysis maps of water pumps in different districts in London that had cholera incidences (Dr.Snowthenaddedthel oc a t i onsofal lt hos ewhoha ddi e df r om c hol e r aont hemap.Andc or r e l at e dt hel o c at i ono ft he vi c t i m’ shome st ot hes our c eo ft he i rdr i nki ngwa t e r . –Apa t t e r ni sr e v e al e d.Hede t e r mi ne dt hatt hema j or i t yo ft hos ewhodi e dhad g ot t e nt he i rdr i nki ngwa t e rf r om t heBr oadSt r e e twat e rpumpandnotf r om badai rc omi ngf r om t hec e me t e r y . Af t e rc l os i ngt hatpump t henumbe rofc as e so fc hol e r adr oppe ddr amat i c al l y .I tt ur ne doutt hatt hes e we rpi pe s , bur i e dabout22f e e tdo wn, whe r el e aki ngi nt o t hes ha l l o wwa t e rwe l l s ;t hes hal l o wwe l l swe r eonl y28f e e tde e p. TheBr oadSt r e e tpumpwasonl yoneo fmanys hal l o wwa t e rwe l l si n London. Thede e pe rwe l l shadat hi c ke rbuffe rofs oi l be t we e nt he m andt hel e aki ngs e we rpi pe sandt he r e f or ewe r el e s sl i ke l yt oge t c ont ami na t e d.ThemapsDr . Sno wmadec ons t i t ut eac l a s s i cus eofg e og r aphi ci nf or mat i o nt odr a we pi de mi ol ogi c alc onc l us i ons . Toda y , wemi g htus et hes amepr i nc i pal st ol o c at et hec aus eofanout br e akofWe s tNi l eVi r us , a vi anflu,o ranune xpl ai ne ds our c eoff ood poi s oni ng. )

79) How did Ewald demonstrate that the nature of the water supply influences the evolution of virulence in cholera? – access of pop to potable water vs toxigenicity in cholera strain 80) What prevents diseases from evolving to be extremely virulent? 81) Why was the 1918 strain of influenza so virulent? – human H1 virus circulating around the 1900s picked up genetic material from bird flu virus just before 1918. Old people were already exposed to a virus like this one so their immune systems were better able to create antibodies than young people 82) How did infectious disease affect the colonization of the Americas by Europeans? 83) How do vaccination ...