Notes from 2/4-2/11
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This 7 page Class Notes was uploaded by America Seach on Thursday February 11, 2016. The Class Notes belongs to BIOL at Clemson University taught by Sears in Spring 2016. Since its upload, it has received 26 views.
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Date Created: 02/11/16
Evolution Notes Exam 2: 2/4/16 - Variation Among Individuals- it is the raw material for evolution o Plants, animals, humans all vary in appearance - Cells are distinguished by the proteins they make: o Red blood cells: hemoglobin to transport oxygen o Goblet cells: digestion o Rod cells: in eye o DNA can have different folding patterns - Vp = Vg + Ve + Vg*e o Phenotypic variation = genotypic variation plus environmental variation plus gene by environment interaction o Genotype variation: different alleles o Environment: depends on food they eat o Gene by environment: can have the same gene but may have different environment - Genetic Variation: there are different alleles for each gene o Taste receptors: PTC- bitter flavor; PAV allele fits into receptor and taste bitterness; AVI allele doesn’t fit into receptor so do not taste bitterness; PAV/PAV= very bitter; PAV/AVI = not too bitter; AVI/AVI= not bitter o Genetic variation consists of differences among individuals that are encoded in the genome and transmitted from parents to offspring - Environmental Variation: occur by changes in the environment o Consists of differences among individuals due to exposure to different environments; one way environments can influence phenotypes is by altering gene expression o Daphnia: if exposed to predator, it grows a horn; if it is not exposed to a predator, it does not grow a horn; phenotypic plasticity - Epigenetics: o “Linnaeus would be proud”- being able to pass changes specifically because of the environmental exposure toadflax shows variation - Gene by environment interaction o Leopard gecko: experience temperature dependent sex determination- temperature experience during birth affects the gender of the gecko; more males produced at moderate temperatures, females at extremes Climate change could cause all male or all female populations Some are sensitive/insensitive to temperature change o Happens in people: have different genotypes for serotonin transporter gene; chances of depressive episodes are more likely if you have ss genotype o Catepillars: most exhibit the black gene, but with heat shock (42 degrees), they start showing more green o What happens if you breed heat shock? o Because of their heritable component, genetic variation and genotype-by-environment interaction are raw material for evolution by natural selection - How do we know what is responsible for phenotypic variation: o Common garden: bringing them to the same temperature; if it is only genetic, it should remain the same size regardless of the change in environment o Reciprocal transplant: swapping location/temperature; maintain the same body size means its genetic only o Common garden ENVIRO ONLY: change location to same one, they line up o Reciprocal transplant: ENVIRO ONLY parallel lines o Common garden and reciprocal transplant (intermediate- gene by environment): don’t align and do not stay the same o Example not in textbook: rufous-collared sparrows: took animals from low and high environments to see what happens; some of the proteins were different but when they group up together to be similar o Can the thermal environment explain geographic patterns of body size? Depending on where you are, the body size changes; more active season creates a larger body size; when you look at the ones in nature- the body sizes were very different (~50%), but grew to normal size after juvenile years Differences were only environmental; variation in body size is not genetic due to the common environment not causing changes in body size - Where new alleles come from: o Arise from alterations to existing alleles o DNA makes copies of itself by complementary base pairing o Sometimes there are spontaneous deamination: methylated cytosines can react with a water to become thymines; mutation that can be passed on throughout generations o Misalignment: the template and nascent DNA strand can slip out of register at repeat sites, resulting in duplications and deletions; hard to come back from o Survival of mice: normal mice live longest, deficient mice do not last as long; and doubly deficient mice live only about 3 months - How mutations alter protein function: o Depends on where mutation is o Point mutation: sometimes just changing the third codon does not affect the amino acid; but changing either first or second can drastically change the amino acid (maybe from polar to nonpolar; acid to base, etc); can affect how it folds o Transversion: purine to pyrimidine o Transition: purine to purine; - Where new genes come from? o Gene duplication: done by unequal crossing over o Duplication by retroposition: introns spliced out then reverse transcription happens, then integration, and final product is new gene o Phylogeny from RNASE1 genes: douc langer is a vegetarian monkey; may have better digestive abilities because of RNASE1B (might have occurred because of unequal crossing over) o Corgis have short legs: comes from DD alleles found in short legged dogs (retropositions- lack introns) o Occurs when genes are formed from scratch because of a change from a stop codon to not a stop codon so have long strand of dna compared to what was intended - Gene duplication is an important category of mutation for evolution. An increase in copy number may itself be adaptive. Duplication followed by divergence in function generates gene families. 2/9/16 - Chromosome Mutations: - Point mutations: single mutation where base pair switches - Chromosome inversions: they suppress crossing over, resulting in ‘super genes’; both ends of the chromosomes break and then are bound back together, but sometimes there are mistakes where they bind to the wrong side of the chromosome; linkage changes- either linked physically or by function- two genes that are closer together are more likely to be inherited together than two that are on opposite ends o Recombination: when they cross over and a chunk from each chromosome goes to the opposite side o Linkage in these areas go up if crossing over doesn’t occur- large portions of chromosomes inherited together - Are they important in evolution? o Flies: we know so much about these flies and they exist out in nature; notice that there’s specific mutations/duplication in certain locations; can tack genomes as they track latitudes (typically associated with climate); same inversions in North America as South America; by linking genes close together and inheriting them together, they might be favored by certain environments—evolve to fit this environment: CLINES o Selection might favor chromosomal inversions to help maintain combinations of alleles across nearby loci - Genome duplications: o Duplications of the entire genome are an important mechanism of speciation—particularly in plants o EX: Diploid parent produces diploid gametes because they can self-fertilize and “back-crosses” to parent; forms an incompatible species and can create a whole new species o Can isolate themselves from a population - Genome duplication as a mechanism of adaption o Changes in ploidy can alter phenotypes in a way that makes individuals better adapted to new environments o Hexads do good in dry environment; neohex did better than tetraploids o Can act on entire genome mutation - Genome duplication can occur in animals too: 1. Female doesn’t incorporate any male genetic material 2. Female incorporates male genes, but increases ploidy levels 3. Female replaces some of her genetic material - rates and fitness effects of mutations: o mutation accumulation experiments demonstrate that mutation rate evolves (putting in a controlled environment) o gene duplication can be more common that mutations o a lot of variation in mutation rates- high mutation rates in viruses o mutation itself is a trait that can evolve - everyone is a mutant: we inherit up to 100 mutations from our parents o in US: males are the ones who cause most mutations o in Nigeria: the egg carries a majority of the mutations - variation between gender, population, location - the distribution of fitness effects of new mutations: site-directed mutagenesis and accumulation o mutated genes randomly and looked at frequency of their mutations and correlations with fitness 20% were lethal, ~half were neutral have ones that are lethal, neutral, beneficial, and somewhat damaging o many of the mutations accumulate lines carried beneficial mutations - mutations come in four kinds: lethal, deleterious, neutral (MOST COMMON), and beneficial o lethal and deleterious mutations outnumber beneficial mutations - the balance between mutation and natural selection o it is the action of natural selection, culling damaging mutations and preserving the advantageous ones, that saves population from inexorable decline o while mutation is random, natural selection acts on these to make more advantageous individuals - Population Genetics: integrates evolution by Darwinian evolution with Mendelian genetics o From a population geneticist’s perspective, evolution can be defined as change across generations in the frequencies of alleles (a copy of a gene). - Frequency of TRYP1 G allele: this G allele decreases drastically - The lifecycle of an idealized population: o We want to know whether particular alleles or genotypes become more common or less common across generations and why o Adults produce gene pool of gametes that are fertilized to zygotes to create a population of juveniles that will grow into adults. (no genetic drift, no mating preference) o Adults choose their mates at random: gene pool with a frequencies of 0.6 for Allele A and 0.4 for allele a - Closing your eyes and picking random alleles o Calculating allele frequency o If not all get to reproduce, the population has to evolve due to “blind luck” - A Numerical Calculation: random mating in the gene pool produces zygotes with these proportions if they are heterozygous: 36% AA, 48% Aa, and 16% aa for 100% total - When chances play no role, the allele frequencies do not change from one generation to the next so no evolution occurs o MAKE SURE IT ALWAYS ADDS TO ONE - Yule vs Punnett: o Yule: when half are A and half are a, then the population is stable o Punnett: the frequency of one allele + the frequency of another allele totals 1. - Hardy-Weinberg Equilibrium Principle: Each person has a p+q so you do (p+q) =1 because it involves diploid; o Conclusion 1: the allele frequencies in a population will not change, generation after generation o Conclusion 2: if the allele frequencies in a population are given by p and q, the genotype frequencies will be given by p , 2pq, and q 2 ASSUME: No selection, no mutation, no migration, no chance events, individuals choose mates at random and population is BIG - if your population is not at equilibrium, one of the assumptions is affecting the population. - A case study: what are the genotype frequencies for the population? o MM: 1787 o MN: 3039 o NN:1303 Add them all up and divide the individual numbers by the total for the population - What are the gene frequencies? o M p= [1787 + (0.5* ) divided by the total population o N q= - Square p for MM, multiply 2pq for MN, and 2/11/16 - Assumptions of Hardy-Weinberg equilibrium: 1. there is no selection 2. there is no mutation (increases variation in population) 3. there is no migration (brings in new variations to change allelic frequencies) 4. there are no chance events (populations are infinitely large) 5. individuals choose their mates at random - Conclusions of H-W equilibrium o P^2 + 2pq + q^2 = 1 o Conclusion 1: the allele frequencies in a population will not change, generation after generation o Conclusion 2: if the allele frequencies in a population are given by p and q, the genotype frequencies will be given by p^2, 2pq, and q^2 - Mechanisms of Evolution: o By providing a set of explicit conditions under which evolution does not happen, the hardy-weinberg analysis identifies the mechanisms that can cause evolution in real populations o Genetic drift (founders effect): small population size causes this o Selection: forces evolution; o Migration: new people come in from another population o Mutation: switching from dominant to recessive alleles or vice versa but are rare - How do we know when a population is not in H-W equilibrium? o Use a statistical test known as CHI-SQUARED - Chi-squared test: o Need a test statistic: take the sum of all phenotype calculations for this formula [(observed-expected)^2] / expected o Degrees of freedom (how many choices you have before you have no more meaningful choices): df = k-1-m (m is alleles) o Cutoff for statistical significance for 1 degree of freedom is 3.841. o EXAMPLE: Need to go to observed frequencies to expected (find values for p and q) P= .62 Q= .38; p^2 =0.384, 2pq= 0.47, q^2= 0.14 AA= 36.6 (p^2*N(total population) 0.384*95) Aa= 44.7 (0.47*95) Aa= 13.3 (0.14*95) Chi-squared: take the (observed- expected)^2 divided by the expected for each genotype; add them together = 0.44 since it is less than 3.841, you can assume its in h-w equilibrium o p value greater or less than 0.05 - Selection: happens when individuals with particular phenotypes survive to sexual maturity at higher rates than those with other phenotypes, or when individuals with particular phenotypes produce more offspring during reproduction than those with other phenotypes - Calculating gene frequencies under selection: incorporating fitness of genotypes o Fitness is denoted as w - Allelic frequency change by Selection: o Flies attracted to alcohol, but it is deadly to them o Flies that grow up in ethanol, changes the frequency of having the fast allele over generations - Selection can change genotype frequencies so that they cannot be calculated by multiplying the allele frequencies. This is an example of OVER-DOMINANT; heterozygote have an advantage over homozygotes - Can human populations evolve in response to HIV? -