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Final Exam Outcomes 13-24.docx

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Western University
Biology 1001A
Tom Haffie

OUTCOMES 13­24 INDEPENDENT STUDY OUTCOMES LECTURE 13 Chapter 10 (10.2, abf, figure 10.15 Chapter 16: 16.1 and 16.2 Genetics of humanABO blood groups • Multiple alleles Blood Type Antigens Antibodies Accepted Transfusions A A Anti-B Aor O B B Anti-A B or O AB Aand B None A, B,AB or O O None Anti-A, anti-B O • Produced by different combinations of multiple (3) alleles of a single gene: Ia, Ib and i • IAIA: type A, Iai: typeA, IaIb = typeAB, IbIb = B, Ibi = B ii = O • Ia and Ib are codominant alleles that are each dominant to the I allele Strategy to distinguish between a phenotype that results from codominance relative to incomplete dominance • Incomplete dominance: effects of recessive alleles can be detected to some extent (intermediate phenotype) – all F1 are pink, and in F2, ½ are pink. The red allele encodes an enzyme the produces a red pigment, but we need enough of it to produce enough of the active form of the enzyme for fully red flowers. The enzyme is completely inactive is homozygous for white plants – colourless flowers that appear white because of the scattering of light by cell walls and other strucutres. With heterozygotes, only product enough pigment to give flowers pink colour. • Some human cells show incomplete dominance: for example, sickle cell disease – alteration in the hemoglobin molecule that changes shape of red blood cells when oxygen levels are low. When someone is heterozygous for this allele they have the trait (still enough of dominant trait) • Alot of diseases have heterozygotes so they appear normal but you need to look at the biochemical level and see that they’re not • Codominance: alles have approximately equal effects in individuals – making them equally detectable. • Characteristics that identify a pleiotropic allele • Single gene affecting more than one character of an organism called pleiotropy • Sickle cell disease: recessive allele of a single gene – but the altered hemoglobin protein can cause serious side-effects • Wide-ranging effects Genetic Variation • Phenotypic variation: differences in appearance or function that – if based on heritable information – are passed from generation to generation • Quantitative variation: individuals differ in small, incremental ways • Qualtiative variation: characters that exist in two or more discrete states and intermediate forms are absent • Polymorphism: discrete variants = poly man, morphos form. • We describe phenotypic polymorphisms quantitatively by calculating the precentege or frequency of each trait • Phenotypic variation can have genetic and environmental causes; only genetically based phenotypic variation is heritable and subject to evolutionary change OUTCOMES 13­24 • Genetic variation arises within populations largely through mutations and genetic recombination. Artifical selection experiments and analyses of protein and DNAsequences reveal that most populations include significant genetic variation. Conditions under which Hardy Weinberg Equilibrium is possible in a population. • Diploid organism: genotype includes 2 alleles at every gene locus; the sum of all alleles is called the gene pool • Genotype frequencies: percentages of individuals possessing each genotype, and then calculate allele frequencies; p for one allele, q for the other • For a gene locus with 3 alleles there are 3 genotype frequencies but only 2 allele frequencies (sums must equal 1) • HWP: null model that defines how evolution does not occur: predict what they would see if a particular factor had no effect; theoretical reference points against which observations can be evaluated • Puzzled by continuous persistence of recessive alleles – wouldn’t they be outdominated? • Genetic equilibrium: point at which neither allele frequencies nor genotype frequencies change in succeeding generations 1. No mutations are occurring 2. The population is closed to migration from other populations 3. Population is infinite in size 4. All genotypes in the populations survive and reproduce equally well 5. Individuals in the population mate randomly with respect to genotypes • If conditions are met: allele freuqencies of the population for an identified gene locus will never change, and the genotype frequencies will stop changing after 1 generation OUTCOMES LECTURE 13 INHERITANCE in POPULATIONS General pathway of eukaryotic membrane protein production. • From chromosomes (alleles) transcribed into 2 different mRNAs, will be spliced out of nucleus, into ribosomes (2 different messages to 2 different ribosomes), ribosomes translate proteins on the rough ER, proteins translate in the ER, to golgi, processed, into vesicles, proteins on membrane General physiology of skin/hair pigmentation. • Pigmented by cells called melanocytes; melanocytes express genes that create melanin, it is stored into organelles called melanosomes • The melanosomes can be filled with black melanin or with red melanin (black or red) – there is no brown. • Those melanosomes get exported out of the melanocytes into skin cells • This one cell can make both colours, kinds of pigments (black or red) Characteristics of dominant alleles. • The one that determines the phenotype in a heterozygote • Always turned “on” – the black allele is always stuck on and therefore always working • Whereas the other allele is sometimes on and sometimes off but even when it’s on it doesn’t matter • It’s dominant not because it’s “fighting” the other - • Dominance is a relationship between gene products produced by different alleles • Whether dominant alleles are more “fit” OUTCOMES 13­24 Which allele in a heterozygote is dominant, given the biochemical mechanism of action of allele products. • Allele products: the dominant allele is one that is always “turned on” – the allele that has its protein receptors always on Factors that do, and do not, affect allele frequencies over time in a population. • Common dominant allele, recessive allele rare: wont change – not a lot of deviation from the starting allele frequencies • Reverse situation: recessive allele common, dominant allele rare - Opposite: also not changing – because there is no selective pressure – you need a selective pressure. Black pigs don’t have higher fitness than red pigs. It is not decreasing in frequency because black pigs are not less fit. • Nothing “magical” about an allele being recessive or dominant that is going to automatically cause it to change in frequency Function of black, brown and red MC1R alleles as described in SimuText. • The gene is called MC1R and the protein product of MC1R is a receptor (a membrane receptor) that detects hormones in the external environment and then signals the internal environment • The “signaling” effects levels of cyclicAMP – very important molecule in biology. In this case, all we care about is when this receptor effects the concentration of cyclicAMP inside the cell • When it’s high we make black melanin • This hormone,ASP, can turn the receptor off – and therefore cyclicAMP levels fall and we produce red melanin • Sometimes the hormone is there, (red) sometimes hormone isn’t there (black) • And that’s where brown comes from – sometimes we make red, sometimes we make black and together that ends up being brown – that’s normal. • The black allele never shuts off; cyclicAMP levels are always very high so the melanocytes always make black melanosomes In the picture, DNAnucleus represents the homologues; MCR1 gene – 2 diferent alleles of that gene on 2 different homologues (brown and black) The chromosomes are in the nucleus; each of those alleles gets transcribed into two different mRNAs, they will splice, leave the nucleus, associate with ribosomes, 2 different messages attaching to two different ribosomes. The ribosomes realize this is a membrane – translate it, carry it to membrane In a heterozygote: has 2 different kinds of receptors on its membrane; because it is expressing 2 different alleles. They are both being expressed. But remember – these organisms were black; the heterozygotes were all black. Well of course they are because the black allele is “stuck” on – it is always working and keeping cyclicAMP levels high and that’s why it’s the dominant one. INDEPENDENT STUDY OUTCOMES LECTURE 14 SELECTION & FITNESS Meaning of gene pool, allele frequency, genotype frequency, genetic equilibrium • Gene pool: Sum of all alleles at all gene loci in all individuals • Genotype frequencies: the percentages of individuals possessing each genotype • Genetic equilibrium: Point at which neither allele frequencies nor genotype frequencies change in succeeding generations Allele frequencies in a population, given the genotype frequencies • Genotype frequencies: OUTCOMES 13­24 • Genotype # of Individuals Genotypic frequencies MM 1787 MM = 1787/6129 = 29 MN 3039 MN = 3039/6129 = 50% NN 1303 NN = 1303/6129 = 21% Total 6129 • Using the total number of individuals (x2) • To deter mine the allelic frequencies we simply count the number of M or N alleles and divide by the total number of alleles. So the allelic frequency for the M allele will be: • f(M) = [(2 x 1787) + 3039]/12,258 = 0.5395 • and the frequency for the N allele will be: • f(N) = [(2 x 1303) + 3039]/12,258 = 0.4605 • By convention one of the alleles is given the designation Pand the other q. Thus for the data we presented above, p=0.5395 and q=0.4605. Because we are analyzing all the alleles, the frequencies shoul d sum to 1.0 and p + q = 1. Genotype frequencies in the next generation, given the allele frequencies and assuming Hardy-Weinberg equilibrium 2 2 • Equation: p + 2pq + q = 1 Conditions necessary for Hardy-Weinberg equilibrium • No mutations • No genetic drift • Non-random mating can’t happen • No migration OUTCOMES LECTURE 14 FITNESS & SELECTION Conditions necessary for Hardy-Weinberg equilibrium • (Previous lecture) Whether a population is in HWE, given observed genotype or phenotype frequencies • Allele frequency: Total alleles R(x2) + alleles r/ calculate the allele frequencies by calculating if there is 1000 individuals, and we know that the population is diploid, there are a total of 2000 alleles in this population of 1000 individuals • Calculating allele frequencies in the future generation: The likelihood of RR - have to inherit an R allele from dad (0.4 from dad and a 0.4 from mom = 0.16/or 16% of the offspring have an RR genotype) For the heterozygotes there are 2 routes to become one • You can inherit the W allele from mom and R allele from dad (0.6x0.4 = 0.24) but you can also inherit R from mom and W from dad (2x0.24) :) p^2 + 2pq + q^2 Relative vs absolute fitness • Fitness describes the ability of an organism to survive and reproduce • Calculated by #offspring/lifetime • Absolute fitness (W) = number of individuals with genotype after selection compared to (ratio) before selection  the number of offspring over a lifetime OUTCOMES 13­24 • Absolute fitness is determined by o Survival to adulthood o Longer they live as adults, more opportunity to product (longevity) o Attracting mates o Fertility o Offspring survival • Can compare genotypes by making assumptions on the above components • First step in estimating strength of selection is to calculate absolute fitness = units = # surviving offspring • Relative fitness = (w); standardization of the absolute fitness to get a relative fitness for a certain genotype. Standardize by comparing to absolute fitness of other individauls in the same population (does not make sense to compare human fitness to fruit fly because the units are so different). Instead, compare the fitness of this genotype of human to the other. How to calculate relative fitness • Calculate W for all the genotypes, Fittest genotype has W = 1 (most successful, genotype with the highest absolute fitness). If you were the fittest genotype your relative fitness is always 1. • Divide absolute fitness of the genotype/absolute fitness of the most successful genotype of Wmax. All other w = W/Wmax; so if absolute fitness (W = 8, and Wmax = 10 for a certain genotype, then w for the genotype = 8/10 = 0.8) • Absolute fitness of aa/Absolute fitness of most successful How to quantify strength of selection • If the difference in w is big = strong selection • Strong selection acts more quickly Relationship between dominance/recessiveness of alleles and response to selection • When selection is going on, it does matter if selection is favoring dominant or recessive allele • Natural selection favors a more beneficial allele • Dominant alleles (if harmful) are more easily removed because they are more frequently found in the genotypes • It takes longer for a favorable recessive allele to spread; less alleles to act on • Black allele (dominant) was favoured by selection; increases in frequency but it may never completely outcompete the harmful, recessive allele. Why is that? Aharmful recessive allele is shielded from selection when it is in the body of a heterozygote individual • Pigs have one copy of B and one copy of R; their fitness is fine – harmful recessive alleles can persist in a population at low frequencies. When they are very rare, most of the copies will be found in heterozygotes of normal fitness – reason for this because when q is really low, q^2 is lower than 2pq. This explains disorders  • Vast majority of disorders are recessive; few dominant genetic disorders associated with a dominant allele but really rare for the most part • Selection against a dominant allele can successfully weed out all the harmful copies, but selection against a harmful recessive allele can only drive it to low frequencies – can see every copy of a harmful dominant allele • Beneficial recessive alleles will eventually reach fixation (reach frequency of 1) whereas beneficial dominant alleles will increase in frequency quickly but may never reach complete fixation OUTCOMES 13­24 INDEPENDENT STUDY OUTCOMES LECTURE 15 SELECTION vs. OTHER EVOLUTIONARY FORCES • Population’s allele frequencies change over time if one or more conditions of model are violated • Processes include mutation, gene flow, genetic drift, natural selection and random mating Mutations create new genetic variations • Mutation is a heritable change in DNA that can be neutral, deleterious or beneficial • Usually rare – so infrequent that they have little/no effect on allele frequencies in most populations • Over evolutionary time numbers are significant; mutations have been accumulating • Major source of heritable, genetic variation • Only mutations in germ line are heritable but in plants mutations in meristem cells are heritable and influence the gene pool • Neutral mutations are neither harmful nor helpful; they can change an organism’s phenotype without influencing its survival and reproduction • Deleterious mutations alter an individual’s structure, function or behaviour in harmful ways • Lethal mutations cause the death of organisms carrying them. If the lethal allele is dominant both homozygous and heterozygous organisms suffer – if recessive, affects only homozygous • Advantageous mutation confers some beefit on an individual; even if the advantage is really slight natural selection can preserve it and increase its frequency How gene flow and genetic drift affect genetic variation within a population, and genetic differences between populations Gene Flow Introduces Novel Genetic Variants into Populations • Organisms or their gametes (like pollen) move from one population to another • If the immigrants reproduce they can introduce new alleles into the population they joined • Gene flow is the name for this and it violates the HW condition that populations must be closed to migration • Common in some animal species • Dispersal agents (pollen-carrying wind or seed-carrying animals) are responsible for gene flow in plant populations • Evolutionary importance of gene flow depends on degree of genetic differentiation between populations and the rate of gene flow between them. For example, if 2 gene pools are very different a little gene flow may increase genetic variability within the population that receives immigrants – it can make them more similar… But if 2 populations are really similar, even a lot of gene flow will have little effect Genetic Drift • Chance events sometimes cause allele frequencies in a population to change unprediactably • Genetic drift is the name; has especially dramatic effects on small populations, which violates HW condition of infinite population size • More pronounced in small populations – for example, if you toss a coin 20/30 times you won’t see the 50/50 ratio like you would if you tossed it 500 times • Chance deviations from expected results, which cause genetic drift, occur when organisms engage in sexual reproduction bc population sizes are not infinitely large. But it’s particularly common in OUTCOMES 13­24 small populations bc only a few individuals contribute to the gene pool + any given allele is present in only a few individuals • Leads to the loss of alleles and reduced genetic variability • Two general circumstances lead to genetic drift: Examples of founder effects and population bottlenecks 1. Population bottlenecks: a stressful factor such as disease, starvation or drought kills many individuals and eliminates some alleles from a population producing a population bottleneck. This reduces genetic variation. Example: hunters wiped out northern elephant seals, since the 1880s the population increased to 30 000 from 20 survivors; but there is barely any genetic variability 2. Founder effect: when a few individuals colonize a distant locality and start a new population, they only carry a few of the parent alleles, so things that were rare in the ancestry might be frequent here and vice-versa. Example: areas in north-eastern Quebec carry a high incidence of myotonic dystrophy – frequency in the rest of the world, allele brought into the region during settlement of the area • Conservation implications: endangered species (small populations) experience severe population bottlenecks = loss of genetic variability Natural Selection Shapes genetic variability by favoring some traits over others • HW model requires all genotypes to survive and reproduce equally well • But some traits enable some individuals to survive and reproduce better • Natural selection is the process – beneficial, heritable traits become more common (HW violated) and frequencies differ from predicted by model • Although natural selection can change allele frequencies, it is the phenotype of an organism rather than the allele that is successful or not • When individuals survive and reproduce, alleles (favorable/unfavorable) are passed on to the next generation • If a lethal allele is recessive it can stay in a population in heterozygous individuals may pass it on to their children • Relative fitness: number of surviving offspring that an individual produces compared with the number left by others in the population (evaluating reproductive success). • Selection is strongest in reproductive life • Measure natural selection by recording changes in the mean and variability of traits in a population over generations – 3 models Examples of directional, stabilizing and disruptive selection 1. Directional selection: traits undero directional selection when individuals near one end of the the phenotypic spectrum have highest relative fitness – shifts a trait away from the existing mean and toward the favoured extreme. The avg changes, but variability probably doesn’t. This is really common. Example: predatory fish promote DS for larger body size in guppies when they selectively feed on the small ones. Humans use DS to produce domestic animals and crops with desired characteristics (small Chihuahuas, and spicy chillis) 2. Stabilizing selection: traits undergo stabilizing selection when individuals expressing intermediate phenotypes have the highest relative fitness. SS eliminates phenotypic extremes and reduces variation and increases the frequency of intermediate phenotypes. This is the most common form. (the mean doesn’t change) Example: Baby mass (optimum weight is where mortality rate is lowest) OUTCOMES 13­24 3. Disruptive selection: Traits undergo disruptive selection when extreme phenotypes have higher relative fitness than intermediate phenotypes. Alleles that produce extreme phenotypes become more common – promote polymorphism. This is much less common. It decreases the frequency of the mean phenotype, but increases freuqencies of the extreme phenotypes. The mean may be unchanged but variability increased. Example: birds with extreme bill lengths survived Sexual Selection often exaggerates showy structures in males • Sexual selection is a special process that fostered the evolution of showy structures like bright feathers or long tables and also established courtship behaviour • There are 2 related processes: intersexual selection – males produce useless structures that females found attractive (selection between males and females), and intrasexual selection – selection based on interactions between same sex – so intimidating structures produces to fend off other men • Sexual selection probably the cause of sexual dimorphism – differences in size/appearance of males and females • Products bizarre – like energy intensive + increased risk of predation feathers How inbreeding and nonrandom mating affect allele frequencies, and how they affect genotype frequencies • HW principle – mates need to be selected randomly • Many organisms do mate unrandomly though • For example, snow geese select mates of own colour • Because individuals with similar genetically based phenotypes mate with each other, next generation has fewer heterozygous offspring than HW predicts (phenotype frequency) • Inbreeding: special form of nonrandom mating – individuals genetically related mtate with each other (self-fertilization in plants). Inbreeding generally increases the frequency of homozygous genotypes and decreases heterozygotes so recessive alleles are more expressed. • Inbreeding does not cause disorders; the increases frequency of homozygotes resulting from inbreeding results in increased frequency of individauls expressing a genetic disorder Outcomes Lecture 15 Selection & other evolutionary mechanisms How heterozygote advantage and heterozygote disadvantage affect genetic variation • If there is a heterozygote advantage the extreme genotypes are likely to lead to polymorphism – balancing selection but maintaining genetic variation whereas homozygotes only have one allele = type of selection that is fundamentally stabilizing; maintains more than one allele in the population for a long period of time • If there is a heterozygote disadvantage one allele (with highest starting frequency) will reach a frequency of 1 and the other 0 ; decreases genetic variation – fundamentally unstabilizing Whether selection always results in evolution • Selection does not always result in evolution • You can have selection that does not result in evolution – it keeps the population stable and unchanging How positive and negative frequency-dependent selection affects genetic variation • In positive frequency-dependent selection the fitness of a genotype increases as it becomes more common and genetic variation is lost OUTCOMES 13­24 • IN negative frequency-dependent selection the fitness of a genotype increases as it becomes rarer promotes high genetic variation within a population Effect of genetic drift on allele frequencies and genetic variation within a population • Genetic drift can cause allele frequencies to change • There is no selective advantage for one allele over another; some will simply be lost and never regained • This removes genetic variation within populations • It exists greater in smaller populations/populations that have a short-lived experience of being small – random sampling and fundamentally unpredictable • Given enough time, one allele will drift to fixation to reach frequency of one and all other alleles reach frequency = zero, removes genetic variation within a population • Two possible options: founder effect or bottleneck theory Effect of genetic drift on variation (differences) between populations • Genetic Drift increases genetic variability between populations; some populations will be missing an allele, others will have a different one… etc Genetic drift can oppose selection – random sampling increases a deleterious allele Whether or not mutations are directed toward the needs of the organism • Mutations are not random nor are they directed – the organism cannot specify what he would “need” more General fitness effects of mutations • Mutations rarely impact fitness • They are simply the third amino acid on a chain, etc, and can still produce the same protein • Alot of DNAdoes not code for stuff so most potential mutatios have little effect on fitness Why most mutations that affect fitness are harmful • If they affect fitness that means Outcomes Lecture 16 Why Sex? General fitness effects of mutations • One of the most important non-adaptive evolution • Only source of new alleles and new genetic material • General effect: most of the time, mutations have no effect on fitness; or very little effect Why most mutations that affect fitness are harmful • Tend to be harmful – if there is a mutation in a coding sequence of a gene resulting in a different order of amino acid those mutations are more likely to make a protein/enzyme function less as the original • Organisms + products are millions of years old of natural selection, extremely well adapted Effect of gene flow on genetic variation within a population • One of the principles of HWE is closed to migration • No new individuals moving in OUTCOMES 13­24 • So when that happens – similar effects to mutation – migration can introduce new alleles into a population • Increases amount of genetic variation within a population Effect of gene flow on variation (differences) between populations • Tends to operate in opposition to natural selection ‘ • Increases genetic variation How various evolutionary forces interact with (reinforce or oppose) one another • Can interact – oppose one another – natural selection choosing an allele that is adapted to the environment • Then a new allele comes in that opposes that, that isn’t well adapted to the selection pressures Reasons why not all living things are perfectly adapted to their environment • Many things can strain/limit effect of selection to produce that perfect organism • Can reduce effect of selection to produce a population where everyone has fittest possible genotype • Dominant status of alleles – can’t weed out every copy of a recessive allele • Frequency-dependent selection can maintain low-fitness genotypes by virtue of being the most common phenotype • Selection requires time • Requires lots of genetic variation to be present, so if the mutation rate is so low/genetic drift has outweight effect of selection such that no genetic variation = constrains ability of selection • Major trade-offs between competing demands – male fish has to survive for long period of time to produce offspring but convince female fish to mate – if way to acquire mates is to be really bright coloured and susceptible to predators then that’s a trade off Relationship between reproduction and sex • Sex is distinct from reproduction • Reproduction can occur without sex • Sexual reproduction is not the default mode of reproduction; organisms can reproduce Effect of sex on genetic variation • Sex contributes to genetic variation by crossing over (recominbation) in meiosis Types of asexual reproduction • Obligately asexual: only reproduce through parathanogenesis (only females in the population) • Facultatively sexual: can go either way and typically avoid reproducing sexually when conditioners are good • Binary fission: (unicellular) produces genetically identical daughter cells • Parthinogenesis: develop a new individual without fertilization • Vegetative propogation: send out a root-like structure to another place that produces another Types of sexual reproduction (monoecious, dioecious, simultaneous vs sequential hermaphroditism) • Monoecious: one household (male and female parts housed in the same organism) – called a hermaphrodite • Dioecious: different parts in different organisms OUTCOMES 13­24 • Have a big chain of many individuals, ones in the middle are acting as males and females • These things are examples of simultaneous hermaphrodites – at the same time both male gonads and female gametes • Other ways of being a hermaphrodite – sequential monoecious; sex change – yet another example of sexually reproducing species but every individual is born belonging to one and then changes Examples and predictions of size-advantage model of sex change • Once females attain a certain body size in blue wrath species they stop producing eggs and instead change to male function in a matter of hours • There is a threshold body size where individuals change sex • Reason why some start as F and switch to M has to do with different selection pressures that sex and sexual reproduction has on males and females • How big of an advantage is there to having a large body size (male vs. female) • Fitness function: the slope or the shape of the relationship between body size (X) and reproductive success (Y) • Big males more successful than small males (not so extreme) but in the space species there is a huge advantage to being large (lay tons of eggs) • If there is a difference in the slope, predict when individuals will be born and change to the other sex • Where the Function crosses – threshold size at expected change in sex • Steeper for females, every individual born male (if small as you are when you’re just born you have less to lose by being male than being male) but when you reach the point where functions cross, large individual as a male you have more to gain by being female – protandry (male first) Taxonomic distribution of sexual reproduction • Look at animals – the situation is radically different than asexual reproduction prevailing in plants – animals reproduce sexually than asexually • Disadvantages of sexual reproduction • Cost of Mating o Use of lots of resources o Broken hearts o Spending time looking for potential mates o Money cost • These can be substantial costs Cost of meiosis • If we could reproduce asexually, we probably would and just clone ourselves – pass on 100% of alleles to offspring • Would be awesome! • Instead, can only pass on 50% of alleles which is only half as efficient in terms of getting alleles into next generation Cost of males • Males contribute a little but in terms of a speed I nwhich population can grow, an all-female population would grow much faster than a solely-male population (blowing half of its resources on males every generation) OUTCOMES 13­24 "Muller's Ratchet" explanation for advantage of sexual reproduction • Sex so widespread that there must be advantages (cost of mating, males, meiosis) • Population level benefit – those that reproduce sexually are able to evolve faster and weed out harmful alleles and combine beneficial mutations • Idea is that populations in which sexual reproduction occurs are less likely to go extinct • Muller’s Ratchet: tool that goes in one direction; harmful mutations accumulate – in asexually reproducing population there is no way of completing losing the harmful mutations; in a sexualy reproducing population you introduce more scatter around this frequency distribution – every time reproduce sexually you are “rolling the dice” and offspring can either have more mutations or get lucky and produce offspring where sex breaks the ratchet – sex can recreate genotypes with very small numbers (or even zero!) of harmful mutations "Ruby in the Rubbish" explanation for advantage of sexual reproduction • “Ruby in the Rubbish” hypothesis: by reproducing sexually you have the option that offspring will be rubbish but you can be lucky and get ruby – lower than average mutation • By continually creating new combinations of alleles you end up with genotypes that have fewer than average harmful mutations – offspring that are better than either of their parents Problem with mutational explanations for advantage of sexual reproduction • Effectively a group selection • Independent Study Outcomes Lecture 17 Sexual Selection i) Chapter 39, pg 981-983. Look at sections "Mates as Resources"; and "Sexual selection". ii) Chapter 16, p 376 (section 16.3e) and 378 (Figure 16.13). Meaning of monogamy, polygamy, polygyny, polyandry, promiscuity, lek Mates as Resources • Mating systems evolved to maximize reproductive success in response to amount of care offspring require and other spects of a species’ecology • Monogamy: mating system male and female form a pair bond either for a mating system or for entire individual’s reproductive life. • Polygamy o One male has active pair bonds with more than one female (polygyny)  males contribute nothing but sperm o One female has active pair bonds with more than one male (polyandry)  females contribute nothing but eggs • Promiscuity: males and females have no pair bonds beyond time it takes to mate • Leks: congregations of displaying males where females come only to mate – kind of like a market place (lekking behavior) Conditions favouring the evolution of monogamous versus polygynous mating systems Favoring monogamy: • Monogamy prevails when young require great deal of care that can be provided from both parents • Males and females achieve higher rates of reproduction when both parents actively involved in raising young • Monogamy occurs in species where males indirectly feed offspring by bringing food to the mother, whereas in mammals the mother can provide food to her young directly (milk) OUTCOMES 13­24 Favoring polygynous: • Males have high-quality territories – role as a sperm donor and protector of the space rather than active parent • Polygyny prevalent among mammals because the females make a larger investment in raising young (eggs and care) Promiscuous mating systems: • Occur when females are only with males long enough to receive sperm – no pair bond • Males make no contribution to feeding the young • Leks: congregations of displaying males where females come only to mate – kind of like a market place (lekking behavior) Handicap explanation for why females prefer males with extravagant ornaments • When males compete for females, males are larger and may have ornaments/weapons – useful for attracting females and warn off rivaling males • Why would females choose males with these exaggerated structures? 1. Man’s large size, bright feathers etc. might show that he is healthy 2. Indicates that he can harvest resources efficiently 3. Managed to survive to an advanced age o All 3 are signals of male quality – and if they reflect genetic makeup he will fertilize the egg with successful alleles • Degree to which females actively choose genetically superior mates varies among species o In some species it is passive = male finds group of females and rivals other males to mate with the female, who struggles during copulation. Other males are attracted to the female struggle and interrupt the current copulation. Only largest and most powerful males are not interrupted o In other species females are more active. They mate only after inspecting several partners. Active female choice most apparent at leks (display grounds for males where each one holds a small territory). Females favor males who come to the lek daily, defend their small area vigorously and display more frequently than the avg lek participant • In general, more elaborate (impressive) features increases offsprings’chance of survival; this is called the handicap hypothesis: females select mates that are successful, the ones with orante structures. The structures may impede locomotion and attract predators but they have survived with them thus far despite the “handicap” – successful alleles responsible for the ornamental handicap are passed to the female’s offspring Meaning of sexual dimorphism, intersexual selection, intrasexual selection • Sexual selection: evolution of showy structures and elaborate courtship behaviour and pushes phenotypes to one extreme • Sexual dimorphism: one gender is larger/more colourful than the other (an outcome of sexual selection) – basically differences in the size/appearance of males and females • Intersexual selection: selection based on the interactions between males and females  produce otherwise useless structures just because females found them attractive in the past • Intrasexual selection: selection based on the interactions between members of the same sex  males use large body size, antlers, tusks to intimidate, injure or kill rival males Figure 16.13 OUTCOMES 13­24 • Is the long tail of the male long-tailed widowbird the product of intrasexual selection, intersexual selection or both? (Checked because long tails are energy intensive to maintain and may increase risk of predation – so why are they so important?) • Outcomes of an experiment: males with experimentally lengthened tails attracted more than twice as many mates as males in the control groups, and shortened tails attracted fewer. No differences in ability of altered males and control group males to maintain display areas. • Conclusion: females prefer the males with lengthened tails and there was no obvious effect on interactions between males – thus it is the product of intersexual selection OUTCOMES LECTURE 17 How and why sexual reproduction increases the speed at which favourable mutations can be combined • In asexual reproduction, beneficial alleles introduced in the population compete against one another • The first has to reach a frequency of one in order for the next to be introduced; altogether this takes a lot longer and only some acquire all 3 • Sexual reproduction can combine multiple alleles in the same individual quickly Relationship between sexual reproduction and extinction risk • Asexual reproduction poses a higher extinction risk • Asexual reproduction cannot weed out harmful alleles • Sexually reproducing populations can adapt to a changing environment and not die out • Any populations who we see are reproducing asexually is a fairly recent change (young species)  there are still vestigial traits of sexual reproduction in species that reproduce asexually Why mutational (long-term) explanations for sex are not sufficient to explain its persistence • This isn’t how natural selection operates • Natural selection is in the “here and now” – what will benef
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