Lecture 19 - Ecology & Evolution Part 1 PDF

Evolution and Ecology Part 1 Time = 8:40 AM  Outline of Ecology & Evolution Part 1 Evolution by natural selection Virulent parasites exert strong natural selection on their hosts and drive the evolution of host immunity Evolution of immunity in house...

Evolution and Ecology Part 1 Time = 8:40 AM  Outline of Ecology & Evolution Part 1 Evolution by natural selection Virulent parasites exert strong natural selection on their hosts and drive the evolution of host immunity Evolution of immunity in house finches to resist mycoplasmosis Evolution of sickle cell mutation in humans to resist malaria parasites Artificial selection for increased productivity in domestic animals has occurred at the expense of disease resistance Broiler chickens selected for fast growth have reduced immunocompetence Dairy cows selected for higher milk yield have higher incidence of mastitis Evolution by natural and artificial selection can be very fast Evolution is change in the heritable characteristics of biological populations over successive generations  Evolution by natural selection Evolution by natural selection example Fox predator that preys on mice Mice have light fur (genotype AA) or dark fur (genotype aa) Light fur provides camouflage in habitat, whereas dark fur does not G1: frequency of each allele is 50% Foxes catch and eat mice with dark fur P(a) declines in mouse population Evolution = change in allele frequency over time; fox is agent of natural selection  Do parasites exert natural selection on their hosts? Parasites can be a Parasites can be a strong force of natural selection on their hosts Squirrelpox virus extirpated red squirrels in UK strong force of MYXV killed 500 million rabbits in 2 years in Australia selection on their Bd reduced abundance of >500 amphibian species hosts Parasites have strong negative effects on host survival and reproduction  Do hosts and their immune systems evolve in response to parasites? Selection for increased host resistance Experimental evolution: select hosts for increased immunity against parasites Host is fruit fly (Drosophila melanogaster) and parasite is parasitoid wasp (Asobara tabida) Wasps lays their eggs inside fruit fly larvae Once wasp egg hatches, the emerging wasp larva usually kills fruit fly larva Fruit fly larvae mount an encapsulation response that kills wasp egg Only 5% of flies in population have this response Evolution of parasitoid Time = 8:50 AM resistance in fruit flies Experimental selection: expose fruit flies to parasitoid wasps for 8 generations Percent of flies with protective immune response increased from 5% to 60% Control line (no selection) did not evolve parasitoid resistance Hosts have genetic variation for immunity and selection can rapidly increase protection against parasites Question 1: Why is frequency of encapsulation response so low in natural populations? Kraaijeveld & Godfray et al. 1997. Nature 389: 278-280 Question 2: Does the low frequency tell us anything about the cost of the defence? Evolution of resistance to mycoplasmosis in house finches  House finches and mycoplasmosis House finches are native to western North America. Introduced to eastern North America in 1940 1990s, new bacterial disease, mycoplasmosis, observed finch populations in eastern North America Agent was Mycoplasma gallisepticum, bacterial pathogen of poultry In 2 years, mycoplasmosis spread across house finch populations in eastern North America House finch populations in western North House finch (Haemorhous mexicanus) America remain disease-free  Transmission and virulence Clinical signs include conjunctivitis and rhinitis -> ocular and nasal discharge Crusts can damage cornea -> blindness. Death results from starvation and predation Direct transmission of M. gallisepticum occurs at feeders or roosting sites Disease emergence associated with 60% decline in house finch populations M. gallisepticum is endemic with prevalence of ~20% in house finch populations Pathogen has high virulence! Strong Hochachka. 2000. PNAS 97: 5303-5306 selection for disease resistance in house finches in eastern North America Evolution of resistance in house finches Compare resistance to M. gallisepticum between finches from Arizona and Alabama Finches from Arizona (western NA) have no experience with mycoplasmosis Finches from Alabama (eastern NA) in 2007 have 12 years of co-existence with disease Experimental infection of disease-free finches with M. gallisepticum in lab Abundance of M. gallisepticum was higher in naïve Arizona finches compared to co- evolved Alabama finches Arizona Alabama Compare gene expression between finches  Evolution of gene expression in finches Disease-induced natural selection will drive evolution of disease resistance genes in host Panel A: Compare gene expression between infected and uninfected birds from Arizona (AZ) and Alabama (AL) populations Panel B: Infection changed expression of 52 genes; 16 are associated with immunity Panel C: Compare expression of 16 genes of infected birds between unevolved (AZ) and evolved (AL) finch populations Panel C: Infection with M. gallisepticum reduces expression of immune genes in AZ finches compared to AL finches M. gallisepticum suppresses immunity! Bonneaud 2011. PNAS Eastern finches have evolved resistance to 108: 7866-7871 this immunosuppression  Survival of finches when infected Arizona and Alabama finches are ancestral versus adapted, respectively Compare survival of ancestral versus adapted finches following experimental infection with M. gallisepticum Finches were infected with M. gallisepticum = Arizona isolates from 5 different years = Alabama Adapted birds had higher survival compared to ancestral birds for later isolates of M. gallisepticum (2007, 2011, 2015) Eastern finches have evolved resistance that enhanced their survival following infection Question: Why is bird survival decreasing with later isolates of M. gallisepticum? Bonneaud 2018 Current Biology 28: 2978-2983 Evolution of resistance to mycoplasmosis in house finches Mycoplasmosis emerged in house finches in eastern North America in 1990s M. gallisepticum has high virulence. Pathogen caused house finch populations in eastern North America to crash. Strong selection for resistance to pathogen in finch populations in in eastern North America House finch populations in western North America have no experience with M. gallisepticum and serve has ancestral, unevolved controls Compared to ancestral populations in Arizona, the evolved populations in Alabama had lower abundance of M. gallisepticum, higher expression of immune genes, and higher survival In 12 years, house finch populations in eastern North America evolved resistance to M. gallisepticum. Evolution by natural selection is fast!  Humans evolved resistance to malaria Time = 9:00 AM  Human sickle cell trait defends against malaria Hosts evolve resistance to parasites Human example is sickle cell defense against malaria parasites Malaria is a mosquito-borne disease caused by protozoan parasites (Plasmodium) Malaria is transmitted by female mosquitoes in Genus Anopheles Malaria parasites live in red blood cells (RBCs) of vertebrate hosts; feed on hemoglobin Parasites burst out and invade new RBCs  Malaria causes high mortality in humans Map shows death rate (per 100,000 individuals) from malaria in 2017 Today: 300 to 700 million people get infected each year Malaria kills 1 to 2 million people each year Plasmodium falciparum has infected human populations for ~100,000 years Malaria parasites have exerted selection on human populations for a long time Source: https://ourworldindata.org/malaria  Sickle cell trait in human populations Human populations have evolved defenses against malaria parasites Sickle cell trait is caused by a mutant version of human gene for hemoglobin Normal gene for hemoglobin = HbA; mutant sickle cell gene = HbS Heterozygotes (HbAS) are protected from malaria compared to homozygotes (HbAA). Homozygotes (HbSS) develop sickle cell disease with morbidity and mortality Sickle cell trait does not prevent infection with Plasmodium, but protects HbAS individuals against disease  Mechanisms by which sickle cell trait protects against malaria In HbAS children, erythrocytes sickle in presence of Plasmodium infection Sickle erythrocytes containing Plasmodium more likely to be removed from circulation by macrophages in spleen Sickle erythrocytes are leaky and contain fewer resources for Plasmodium Plasmodium changes outer surface of normal erythrocytes to enhance cytoadherence and rosette formation, which cause cerebral malaria Sickle erythrocytes have reduced cytoadherence and rosette formation reducing risk of cerebral malaria Gong et al. 2013. Malaria Journal: 317  Children with AS genotype have lower parasitemia in blood than children with AA genotype Compare malaria parasite density in blood of children with AA and AS genotypes Children categorized according to disease severity: symptomless parasitemia, mild clinical malaria, hospital admission Malaria parasite density in blood was lower in AS children compared to AS children Sickle cell trait controls malaria parasite density in blood Lower parasite levels in children with AS genotype reduce disease severity Williams et al. 2005. JID192(1): 178–186  Children with AS genotype are protected against malaria Genotype AA AS 60 Compare incidence of malaria between children that are homozygous (HbAA) Incidence (no. of episodes/1000 cyfu) versus heterozygous (HbAS) 40 Incidence is number of malaria episodes per 1000 child years of follow-up (cyfu) Incidence of all malaria was reduced by 75% in children with AS genotype 20 Incidence of cerebral malaria was reduced by 86% in children with AS genotype Incidence of severe malarial anemia was 0 reduced by 90% in AS children All malaria All severe malaria Cerebral malaria Severe malarial anemia Convulsions Malarial diseases Sickle cell trait protects children against all types of malaria Williams et al. 2005. JID192(1): 178–186  Distribution of malaria and sickle cell trait Distribution of sickle cell trait in human (red) populations is congruent with distribution of malaria (green) Geographic association provides strong evidence that sickle cell trait has evolved to protect humans from malaria infection J.B.S. Haldane in 1949 suggested that sickle cell trait protects humans against malaria Sickle cell trait was first example of a human adaptation by natural selection Question: Why is the the HbS allele not fixed in human populations? Artificial selection shows power of evolution  Time = 9:10 AM Artificial selection for productivity in farm animals Humans have selected farm animals for increased productivity Examples include increased body weight in broiler chickens 1948: Great Atlantic & Pacific Tea Company sponsored contest to develop superior meat-type chickens Selected for broader breasts, less feathers, increased docility, increased feed-to-meat ratio Today, chickens convert ~2 lbs of feed into 1 lb of meat. Chick develops into 5-lb broiler in 6 weeks Selection for performance versus immunity and disease resistance  Growth-immunity trade-off in broilers Selection for rapid growth in poultry may compromise immunocompetence Meta-analysis on 14 published studies on growth-immunity trade-off in poultry Compare disease resistance between lines selected for fast growth versus control lines with slower growth Measure immune response to antigens or mortality to poultry diseases 13/14 studies found fast growing poultry lines had reduced resistance/immune van der Most. 2011. Functional Ecology 25: 74–80 function compared to control lines Selection for milk yield in dairy cows Genetic selection for increased milk yield in dairy cows has increased global milk production Graph shows milk yield over 305 days has increased from 1960 to 2020 dairy breeds Holstein breed: milk yield increased from 5,000 kg in 1960 to 11,000 kg in 2020 Average milk production per cow has also increased because of improvements in nutrition and management New technologies also important (e.g., automated calf feeders, cow activity Brito 2021 Animal monitors, and automated milking systems)  Mastitis in dairy cows Bovine mastitis is most common disease in dairy cattle in USA and worldwide USA: annual losses of 1.7–2 billion USD Bovine mastitis is inflammation of udder tissue due to microorganism infections Bacterial agents: Pseudomonas aeruginosa, Staphylococcus aureus, S. epidermidis, Streptococcus agalactiae, etc. Clinical signs in udder include swelling, heat, redness, hardness, or pain Relationship between milk production and mastitis in dairy cattle Selection for milk yield Heringstad 2007 J. Dairy Sci. 90: 2419–2426 increased mastitis Selection on Norwegian red cows to study relationship between milk yield and mastitis High Milk Production Cows were selected for high milk production High Protein Yield (HMP), low milk production (LMP), high protein yield (HPY) and low clinical mastitis (LCM) over 5 generations Frequency of clinical mastitis increased in Low Milk Production lines selected for high milk production (HMP) and high protein yield (HPY) Frequency of clinical mastitis decreased in Low Clinical Mastitis lines selected for low clinical mastitis (LCM) No effect of selection for low milk production (LMP) on clinical mastitis Selection for higher milk production makes cows more susceptible to clinical mastitis Artificial selection and inbreeding Artificial selection for productivity drives inbreeding in 6 major US dairy breeds Causes of inbreeding are numerous Intensive selective breeding for limited number of traits Elimination of external environment Adoption of same breeds worldwide Globalization of breeding programs Population genetic diversity is important for long-term success of dairy industry Populations with low genetic diversity Brito 2021 Animal cannot respond to new pathogens or environmental pressures  Artificial selection and disease resistance Artificial selection for productivity in farm animals can reduce disease resistance Farm animals also have reduced genetic diversity to deal with new pathogens and are often maintained at very high densities Pathogens do very well in host populations with high density, low genetic variation, and poor immunity Intensive animal farming is highly dependent on antibiotics and vaccines to protect animals from infectious disease Overuse of antibiotics in agriculture creates other problems  Summary of Ecology & Evolution Part 1 Virulent parasites exert selection on their hosts Fast evolution of resistance in fruit flies to parasitoid wasps Finches in eastern USA evolved resistance to mycoplasma in 12 years Humans evolved sickle cell trait in response to malaria Evolution by artificial selection in domestic animals Selection for productivity can compromise disease resistance (trade-off) Broiler chickens selected for fast growth are susceptible to pathogens Dairy cows selected for high milk yield are more susceptible to mastitis Evolution by natural and artificial selection can be very fast 9:20 AM End of lecture 19  Evolution as History Evolutionary theory consists of history and mechanisms History of evolution is a historical fact Organisms are related to each other via common descent Earth is 4.54 billion years old Life emerged on Earth ~3.7 bya Multicellular life arrive 600 mya Dinosaurs existed from 252 mya to 66 mya Mammals evolved 252 mya to 201 mya Humans evolved 300,000 years Evolutionary tree of life Darwin proposed the idea of the tree of life Tree of life: all organisms related to each other via line of common descent Humans share common ancestor with chimpanzees and other primates Humans share common ancestor with all mammals, with all vertebrates, etc Evidence: organisms can be put in groups based on shared morphological traits Molecular revolution shown that evolution by common descent written in DNA  Mechanisms of Evolution Mechanisms of evolution are processes responsible for creating new species and diversity of life Mechanisms of evolution include mutation, natural selection, genetic drift, and genetic exchange between populations  Darwin & “The Origin of Species” Darwin published his book “On the Origin of Species” in 1859 Many biologists accepted idea of common descent and evolution as historical fact Darwin’s mechanism of natural selection was controversial Mechanism of heredity was solved by Gregor Mendel and others 1920: Theory of evolution was put on firm mechanistic and theoretical footing  Evolution by Natural Selection Variation in phenotype – some individuals are susceptible to infectious disease whereas others are resistant Natural selection (covariance between fitness and phenotype) – when exposed to the infectious disease, susceptible phenotypes have reduced fitness compared to resistant phenotypes Variation in phenotype is heritable – there is variation in the genes (i.e., alleles) coding for immunity that confer susceptibility or resistance to infectious disease  Molecular data and evolution of mammals Evolution of mammals Morphology and molecular biology largely agree with respect to the monophyly of the 18 placental orders Molecular tree recognizes four major clades: Afrotheria, Xenarthra, Laurasiatheria, and Euarchontoglires Afrotheria: elephants, rock hyraxes, manatees & dugongs Euarchontoglires: primates, rabbits & hares, and rodents Laurasiatheria: carnivores, odd-toed ungulates, even-toed ungulates, whales & dolphins, and bats Springer et al. 2004. TREE 19(8)  Rare genomic changes Rare genomic changes (RGCs) include insertions, deletions, changes in gene order, gene duplications, etc. RGCs are important in phylogenetic analysis of DNA sequence data RGCs are rare and therefor they are excellent markers of common descent Members of Euarchontoglires (human, flying lemur, tree shrew, rabbit/hare, mouse) all share 18 AA deletion in gene encoding stem cell antigen-1 protein Members of Afrotheria (sea cow, elephant, Springer et al. 2004. TREE 19(8) hyrax, aardvark) all share a 9-bp deletion in BRCA1 gene